Conflicting social norms and community conservation compliance

Though the success of conservation initiatives relies on changing behaviour, little social psychological research has examined factors such as attitudes and social norms in the context of actual conservation campaigns. In the context of reducing light pollution around sea turtle nesting habitats, researching technological solutions has clear merit. Problems such as light glow are, however, fundamentally about human behaviour, and so finding ways to effect behavioural change is critical. Social norms, or perceptions about what other people think and do, have been widely used in behaviour change campaigns across various domains, including campaigns to promote conservation behaviour. Here, we investigate how the norms of different groups may influence our behaviour in the context of a campaign to alter behavioural norms about light glow pollution in a community. We examine attitudes, social norms, and the degree of conflict (versus congruence) between the behaviours of different groups, and their relationship with intentions to engage in conservation behaviours relevant to sea turtle conservation. We show that attitudes and norms are related to behavioural intentions, and conflicts between social norms influence intentions, over and above the norms themselves. This highlights an important consideration for conservation campaigns utilising social norms-based behaviour change appeals.     

Heritabilities,social environment effects and genetic correlations of social behaviours in a cooperatively breeding vertebrate

Social animals interact frequently with conspecifics, and their behaviour is influenced by social context, environmental cues and the behaviours of interaction partners, allowing for adaptive, flexible adjustments to social encounters. This flexibility can be limited by part of the behavioural variation being genetically determined. Furthermore, behaviours can be genetically correlated, potentially constraining independent evolution. Understanding social behaviour thus requires carefully disentangling genetic, environmental, maternal and social sources of variations as well as the correlation structure between behaviours. Here, we assessed heritability, maternal, common environment and social effects of eight social behaviours in Neolamprologus pulcher, a cooperatively breeding cichlid. We bred wild‐caught fish in a paternal half‐sibling design and scored ability to defend a resource against conspecifics, to integrate into a group and the propensity to help defending the group territory (“helping behaviour”). We assessed genetic, social and phenotypic correlations within clusters of behaviours predicted to be functionally related, namely “competition,” “aggression,” “aggression‐sociability,” “integration” and “integration‐help.” Helping behaviour and two affiliative behaviours were heritable, whereas there was little evidence for a genetic basis in all other traits. Phenotypic social effects explained part of the variation in a sociable and a submissive behaviour, but there were no maternal or common environment effects. Genetic and phenotypic correlation within clusters was mostly positive. A group's social environment influenced covariances of social behaviours. Genetic correlations were similar in magnitude but usually exceeding the phenotypic ones, indicating that conclusions about the evolution of social behaviours in this species could be provisionally drawn from phenotypic data in cases where data for genetic analyses are unobtainable.     

Communication networks: social environments for receiving and signalling behaviour

Communication and social behaviour are inextricably linked, with communication mediating important social behaviours such as resource defence and mate attraction. However, the social environment in which communication occurs is often ignored in discussions of communication behaviour. We argue that networks of several individuals are the common social environment for communication behaviour. The consequences for receivers and signallers of communicating in a network environment are the main subjects of this review. Eavesdropping is a receiving behaviour that is only possible in the environment of a network and therefore we concentrate on this behaviour. The main effect of communication networks on signallers is to create competition with other signallers for receiver attention. We discuss the consequences of such competition. To conclude, we explore the role of signals and signalling interactions as sources of information that animals exploit to direct their behaviour. Received: 1 December 1999 / Received in revised form: 18 January 2000 / Accepted: 18 January 2000     

Fish as a model in social neuroscience: conservation and diversity in the social brain network

Mechanisms for fish social behaviours involve a social brain network (SBN) which is evolutionarily conserved among vertebrates. However, considerable diversity is observed in the actual behaviour patterns amongst nearly 30000 fish species. The huge variation found in socio-sexual behaviours and strategies is likely generated by a morphologically and genetically well-conserved small forebrain system. Hence, teleost fish provide a useful model to study the fundamental mechanisms underlying social brain functions. Herein we review the foundations underlying fish social behaviours including sensory, hormonal, molecular and neuroanatomical features. Gonadotropin-releasing hormone neurons clearly play important roles, but the participation of vasotocin and isotocin is also highlighted. Genetic investigations of developing fish brain have revealed the molecular complexity of neural development of the SBN. In addition to straightforward social behaviours such as sex and aggression, new experiments have revealed higher order and unique phenomena such as social eavesdropping and social buffering in fish. Finally, observations interpreted as ‘collective cognition’ in fish can likely be explained by careful observation of sensory determinants and analyses using the dynamics of quantitative scaling. Understanding of the functions of the SBN in fish provide clues for understanding the origin and evolution of higher social functions in vertebrates.     

Oxytocin, vasopressin and pair bonding: implications for autism

Understanding the neurobiological substrates regulating normal social behaviours may provide valuable insights in human behaviour, including developmental disorders such as autism that are characterized by pervasive deficits in social behaviour. Here, we review the literature which suggests that the neuropeptides oxytocin and vasopressin play critical roles in modulating social behaviours, with a focus on their role in the regulation of social bonding in monogamous rodents. Oxytocin and vasopressin contribute to a wide variety of social behaviours, including social recognition, communication, parental care, territorial aggression and social bonding. The effects of these two neuropeptides are species-specific and depend on species-specific receptor distributions in the brain. Comparative studies in voles with divergent social structures have revealed some of the neural and genetic mechanisms of social-bonding behaviour. Prairie voles are socially monogamous; males and females form long-term pair bonds, establish a nest site and rear their offspring together. In contrast, montane and meadow voles do not form a bond with a mate and only the females take part in rearing the young. Species differences in the density of receptors for oxytocin and vasopressin in ventral forebrain reward circuitry differentially reinforce social-bonding behaviour in the two species. High levels of oxytocin receptor (OTR) in the nucleus accumbens and high levels of vasopressin 1a receptor (V1aR) in the ventral pallidum contribute to monogamous social structure in the prairie vole. While little is known about the genetic factors contributing to species-differences in OTR distribution, the species-specific distribution pattern of the V1aR is determined in part by a species-specific repetitive element, or 'microsatellite', in the 5' regulatory region of the gene encoding V1aR (avpr1a). This microsatellite is highly expanded in the prairie vole (as well as the monogamous pine vole) compared to a very short version in the promiscuous montane and meadow voles. These species differences in microsatellite sequence are sufficient to change gene expression in cell culture. Within the prairie vole species, intraspecific variation in the microsatellite also modulates gene expression in vitro as well as receptor distribution patterns in vivo and influences the probability of social approach and bonding behaviour. Similar genetic variation in the human AVPR1A may contribute to variations in human social behaviour, including extremes outside the normal range of behaviour and those found in autism spectrum disorders. In sum, comparative studies in pair-bonding rodents have revealed neural and genetic mechanisms contributing to social-bonding behaviour. These studies have generated testable hypotheses regarding the motivational systems and underlying molecular neurobiology involved in social engagement and social bond formation that may have important implications for the core social deficits characterizing autism spectrum disorders.     

SLP-2 interacts with prohibitins in the mitochondrial inner membrane and contributes to their stability

Stomatin is a member of a large family of proteins including prohibitins, HflK/C, flotillins, mechanoreceptors and plant defense proteins, that are thought to play a role in protein turnover. Using different proteomic approaches, we and others have identified SLP-2, a member of the stomatin gene family, as a component of the mitochondria. In this study, we show that SLP-2 is strongly associated with the mitochondrial inner membrane and that it interacts with prohibitins. Depleting HeLa cells of SLP-2 lead to increased proteolysis of prohibitins and of subunits of the respiratory chain complexes I and IV. Further supporting the role of SLP-2 in regulating the stability of specific mitochondrial proteins, we found that SLP-2 is up-regulated under conditions of mitochondrial stress leading to increased protein turnover. These data indicate that SLP-2 plays a role in regulating the stability of mitochondrial proteins including prohibitins and subunits of respiratory chain complexes.     

Social interactions in kittiwake colonies: social facilitation and/or favourable social environment

A video study of social facilitation was carried out on a kittiwake, Rissa tridactyla, colony. For the analysis, the video sequences were divided into adjacent periods of 15 s. The temporal limits of each behaviour could thus be defined and its length taken into account. There were significant differences between the behaviour of neighbouring birds during the mating of a pair and that shown at other times. A comparison of the frequencies of behaviours shown by neighbouring birds during the two alternating stages of mating (Mounting and Copulation) permitted two kinds of behaviours, which differed during mating, to be distinguished. (1) The behaviours that differed between Copulation and Mounting reveal the reaction of the neighbouring birds to Copulation (but no evidence of social facilitation could be found). (2) The behaviours that differed only between Mating sequences (case sequences) and other sequences (control sequences) had probably started before the mating started. Consequently, the temporal clustering of activities in colonies may be due to the effect of particular behaviours which could favour the appearance of certain other behaviour. This mechanism (Favourable Social Environment) can act simultaneously with social facilitation. It raises the possibility that social environment may influence greatly the production of young in colonial birds.     

Cooperative personalities and social niche specialization in female meerkats

The social niche specialization hypothesis predicts that group‐living animals should specialize in particular social roles to avoid social conflict, resulting in alternative life‐history strategies for different roles. Social niche specialization, coupled with role‐specific life‐history trade‐offs, should thus generate between‐individual differences in behaviour that persist through time, or distinct personalities, as individuals specialize in particular nonoverlapping social roles. We tested for support for the social niche specialization hypothesis in cooperative personality traits in wild female meerkats (Suricata suricatta) that compete for access to dominant social roles. As cooperation is costly and dominance is acquired by heavier females, we predicted that females that ultimately acquired dominant roles would show noncooperative personality types early in life and before and after role acquisition. Although we found large individual differences in repeatable cooperative behaviours, there was no indication that individuals that ultimately acquired dominance differed from unsuccessful individuals in their cooperative behaviour. Early‐life behaviour did not predict social role acquisition later in life, nor was cooperative behaviour before and after role acquisition correlated in the same individuals. We suggest that female meerkats do not show social niche specialization resulting in cooperative personalities, but that they exhibit an adaptive response in personality at role acquisition.     

Polymorphism at the avpr1a locus in male prairie voles correlated with genetic but not social monogamy in field populations

Integrative studies of genetics, neurobiology and behaviour indicate that polymorphism in specific genes contributes to variation observed in some complex social behaviours. The neuropeptide arginine vasopressin plays an important role in the regulation of a variety of social behaviours, including social attachment of males to females, through its action on the vasopressin 1a receptor (V1aR). In socially monogamous prairie voles ( Microtus ochrogaster ), polymorphism in the length of microsatellite DNA within the regulatory region of the gene ( avpr1a ) encoding the V1aR predicts differences among males in neural expression of V1aRs and partner preference under laboratory conditions. However, understanding the extent to which V1aR mediates variation in prairie vole social and reproductive behaviour observed in nature requires investigating the consequences of avpr1a polymorphism and environmental influences under ecologically relevant conditions. We examined the relationship between avpr1a length polymorphism and monogamy among male prairie voles living in 0.1 ha enclosures during a time similar to their natural lifespan. We found no evidence that avpr1a genotype of males predicts variation in social monogamy measured in the field but some indices of social monogamy were affected by population density. Parentage data indicated that a male's avpr1a genotype significantly influenced the number of females with which he sired offspring and the total number of offspring sired. Total brain concentrations of V1aR mRNA were not associated with either male behaviour or avpr1a genotype. These data show that melding ecological field studies with neurogenetics can substantially augment our understanding of the effects of genes and environment on social behaviours.     

Mitochondrial genome evolution in the social amoebae

Most mitochondria contain a core set of genes required for mitochondrial function, but beyond this base there are variable genomic features. The mitochondrial genome of the model species Dictyostelium discoideum demonstrated that the social amoebae mitochondrial genomes have a size between those of metazoans and plants, but no comparative study of social amoebae mitochondria has been performed. Here, we present a comparative analysis of social amoebae mitochondrial genomes using D. discoideum, Dictyostelium citrinum, Dictyostelium fasciculatum, and Polysphondylium pallidum. The social amoebae mitochondria have similar sizes, AT content, gene content and have a high level of synteny except for one segmental rearrangement and extensive displacement of tRNAs. From the species that contain the rearrangement, it can be concluded that the event occurred late in the evolution of social amoebae. A phylogeny using 36 mitochondrial genes produced a well-supported tree suggesting that the pairs of D. discoideum/D. citrinum and D. fasciculatum/P. pallidum are sister species although the position of the root is not certain. Group I introns and endonucleases are variable in number and location in the social amoebae. Phylogenies of the introns and endonucleases suggest that there have been multiple recent duplications or extinctions and confirm that endonucleases have the ability to insert into new areas. An analysis of dN/dS ratios in mitochondrial genes revealed that among groups of genes, adenosine triphosphate synthase complex genes have the highest ratio, whereas cytochrome oxidase and nicotinamide adenine dinucleotide (NADH) dehydrogenase genes had the lowest ratio. The genetic codes of D. citrinum, P. pallidum, and D. fasciculatum are the universal code although D. fasciculatum does not use the TGA stop codon. In D. fasciculatum, we demonstrate for the first time that a mitochondrial genome without the TGA stop codon still uses the release factor RF2 that recognizes TGA. Theories of how the genetic code can change and why RF2 may be a constraint against switching codes are discussed.     

Behavioural mating displays depend on mitochondrial function: a potential mechanism for linking behaviour to individual condition

Males of many animal species court females using complex behavioural displays that are challenging to produce, and some of these displays have been shown to be associated with aspects of male quality. However, the mechanisms by which behavioural displays are linked to individual condition remain uncertain. Herein, we illustrate fundamental mechanistic connections between mitochondrial function and neurogenesis, energy production, and a variety of pathways that underlie the ability of an individual to perform complex behaviours. We consider the biomedical evidence for how mitochondrial activity shapes neurogenesis during development and neural function in adulthood, and how both genetics and environmental conditions can cause variation in mitochondrial function in wild animals. An individual's mitochondrial phenotype determines not just metabolism and available energy, but also appears to serve as an important driver of capacity to perform cognitively complex and other challenging display behaviours. We apply this concept to the example of birdsong, a well‐studied display behaviour with known links to neural pathways, and we describe how mitochondrial involvement in a variety of important internal processes creates links between display quality and key traits like immunocompetence. By synthesizing the intimate involvement of mitochondria in neural processes with the physiological bases of display behaviour, we aim to provide new mechanistic explanations for information that females may gain by assessing complex male displays.     

The social nature of primate cognition

The hypothesis that the enlarged brain size of the primates was selected for by social, rather than purely ecological, factors has been strongly influential in studies of primate cognition and behaviour over the past two decades. However, the Machiavellian intelligence hypothesis, also known as the social brain hypothesis, tends to emphasize certain traits and behaviours, like exploitation and deception, at the expense of others, such as tolerance and behavioural coordination, and therefore presents only one view of how social life may shape cognition. This review outlines work from other relevant disciplines, including evolutionary economics, cognitive science and neurophysiology, to illustrate how these can be used to build a more general theoretical framework, incorporating notions of embodied and distributed cognition, in which to situate questions concerning the evolution of primate social cognition.     

Targeting proteomics to investigate metastasis-associated mitochondrial proteins

Mitochondria are essential organelles in eukaryotic cells and are responsible for regulating energy metabolism, ROS production, and cell survival. Recently, various cellular pathogeneses, including tumorigenesis and metastasis, have been reported to be associated with mitochondrial homeostasis. Consequently, exploiting the correlation between dysfunctional mitochondria and tumor progression has been implicated in the understanding of tumorigenesis, tumor metastasis, and chemoresistance, along with novel strategies to develop cancer therapeutics. To comprehensively understand the role of the mitochondria in cancer metastasis, it is necessary to resolve thousands of mitochondrial proteins and their post-translational modifications with high-throughput global assessments. We introduce mitochondrial proteomic strategies in this review and a discussion on their recent findings related to cancer metastasis. Additionally, the mitochondrial respiratory chain is believed to be a major site for ROS production, and elevated ROS is likely a key source to trigger dysfunctional mitochondria and impaired mitochondrial metabolism that subsequently contribute to the development of cancer progression. Equipment-based metabolomic analysis now allows the monitoring of disease progression and diagnosis. These newly emerging techniques, including proteomics, redox-proteomics, and metabolomics, are described in this review.     

The enteropathogenic Escherichia coli (EPEC) Map effector is imported into the mitochondrial matrix by the TOM/Hsp70 system and alters organelle morphology

Enteropathogenic Escherichia coli (EPEC) is a human intestinal pathogen and a major cause of diarrhoea, particularly among infants in developing countries. EPEC target the Map and EspF multifunctional effector proteins to host mitochondria - organelles that play crucial roles in regulating cellular processes such as programmed cell death (apoptosis). While both molecules interfere with the organelles ability to maintain a membrane potential, EspF plays the predominant role and is responsible for triggering cell death. To learn more about the Map-mitochondria interaction, we studied Map localization to mitochondria with purified mitochondria (from mammalian and yeast cells) and within intact yeast. This revealed that (i) Map targeting is dependent on the predicted N-terminal mitochondrial targeting sequence, (ii) the N-terminal 44 residues are sufficient to target proteins to mitochondria and (iii) Map import involves the mitochondrial outer membrane translocase (Tom22 and Tom40), the mitochondrial membrane potential, and the matrix chaperone, mtHsp70. These results are consistent with Map import into the mitochondria matrix via the classical import mechanism. As all known, Map-associated phenotypes in mammalian cells are independent of mitochondrial targeting, this may indicate that import serves as a mechanism to remove Map from the cytoplasm thereby regulating cytoplasmic function. Intriguingly, Map, but not EspF, alters mitochondrial morphology with deletion analysis revealing important roles for residues 101-152. Changes in mitochondrial morphology have been linked to alterations in the ability of these organelles to regulate cellular processes providing a possible additional role for Map import into mitochondria.     

Angiogenic activity of mitochondria; beyond the sole bioenergetic organelle

Angiogenesis is a complex process that involves the expansion of the pre-existing vascular plexus to enhance oxygen and nutrient delivery and is stimulated by various factors, including hypoxia. Since the process of angiogenesis requires a lot of energy, mitochondria play an important role in regulating and promoting this phenomenon. Besides their roles as an oxidative metabolism base, mitochondria are potential bioenergetics organelles to maintain cellular homeostasis via sensing alteration in oxygen levels. Under hypoxic conditions, mitochondria can regulate angiogenesis through different factors. It has been indicated that unidirectional and bidirectional exchange of mitochondria or their related byproducts between the cells is orchestrated via different intercellular mechanisms such as tunneling nanotubes, extracellular vesicles, and gap junctions to maintain the cell homeostasis. Even though, the transfer of mitochondria is one possible mechanism by which cells can promote and regulate the process of angiogenesis under reperfusion/ischemia injury. Despite the existence of a close relationship between mitochondrial donation and angiogenic response in different cell types, the precise molecular mechanisms associated with this phenomenon remain unclear. Here, we aimed to highlight the possible role of mitochondria concerning angiogenesis, especially the role of mitochondrial transport and the possible relation of this transfer with autophagy, the housekeeping phenomenon of cells, and angiogenesis.     

Astrocyte Mitochondria in White-Matter Injury

This review summarizes the diverse structure and function of astrocytes to describe the bioenergetic versatility required of astrocytes that are situated at different locations. The intercellular domain of astrocyte mitochondria defines their roles in supporting and regulating astrocyte-neuron coupling and survival against ischemia. The heterogeneity of astrocyte mitochondria, and how subpopulations of astrocyte mitochondria adapt to interact with other glia and regulate axon function, require further investigation. It has become clear that mitochondrial permeability transition pores play a key role in a wide variety of human diseases, whose common pathology may be based on mitochondrial dysfunction triggered by Ca²⁺ and potentiated by oxidative stress. Reactive oxygen species cause axonal degeneration and a reduction in axonal transport, leading to axonal dystrophies and neurodegeneration including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease. Developing new tools to allow better investigation of mitochondrial structure and function in astrocytes, and techniques to specifically target astrocyte mitochondria, can help to unravel the role of mitochondrial health and dysfunction in a more inclusive context outside of neuronal cells. Overall, this review will assess the value of astrocyte mitochondria as a therapeutic target to mitigate acute and chronic injury in the CNS.

     

Adaptation and the genetics of social behaviour

In recent years much progress has been made towards understanding the selective forces involved in the evolution of social behaviour including conflicts over reproduction among group members. Here, I argue that an important additional step necessary for advancing our understanding of the resolution of potential conflicts within insect societies is to consider the genetics of the behaviours involved. First, I discuss how epigenetic modifications of behaviour may affect conflict resolution within groups. Second, I review known natural polymorphisms of social organization to demonstrate that a lack of consideration of the genetic mechanisms involved may lead to erroneous explanations of the adaptive significance of behaviour. Third, I suggest that, on the basis of recent genetic studies of sexual conflict in Drosophila, it is necessary to reconsider the possibility of within-group manipulation by means of chemical substances (i.e. pheromones). Fourth, I address the issue of direct versus indirect genetic effects, which is of particular importance for the study of behaviour in social groups. Fifth, I discuss the issue of how a genetic influence on dominance hierarchies and reproductive division of labour can have secondary effects, for example in the evolution of promiscuity. Finally, because the same sets of genes (e.g. those implicated in chemical signalling and the responses that are triggered) may be used even in species as divergent as ants, cooperative breeding birds and primates, an integration of genetic mechanisms into the field of social evolution may also provide unifying ideas.     

心衰进程中非编码RNA对线粒体功能的调控作用

心衰长久以来一直缺少有效治疗方法,给社会造成了巨大的经济和民生负担,新诊断标志物的确认和治疗方法的研发十分迫切。线粒体功能障碍与心衰发生和发展密切相关,以线粒体为基础的能量供应紊乱、钙失衡、氧化应激和细胞死亡在心衰的发展中起着重要作用,但线粒体调控的具体机制还不十分清楚。非编码RNA被证实在表观调控、转录后修饰、翻译调节等多方面发挥重要调控作用。研究表明,包括miRNA、lncRNA、circRNA在内的大量非编码RNA在心脏发育和心脏疾病发展过程中存在差异表达,并在线粒体蛋白稳态、氧化磷酸化、氧化应激、凋亡与自噬等调控中发挥了重要作用,进而影响心衰等心脏疾病的发生发展,但其详细机制尚未完全阐明。本文就近年心衰发生和发展过程中非编码RNA调控线粒体功能机制的相关研究进行综述,梳理了近年来非编码RNA在调节线粒体结构与功能进而影响心衰发展方面的研究进展,以期为心衰研究与治疗提供新的思路和靶点。     

Culture and courtship in vertebrates: a review of social learning and transmission of courtship systems and mating patterns

Female and male animals often choose mates based upon the complementarity of their courtship behaviours and preferences. The importance of this fact on the evolutionary dynamics of populations has long been appreciated. What has not been appreciated is the role that social learning might play in the transmission of systems of courtship behaviour across generations. This paper addresses the social transmission of courtship behavioural traditions in vertebrates. It discusses views of culture in the context of behavioural signals and preferences in courtship. It then reviews empirical evidence for culture-like processes affecting courtship behaviour, focusing on studies of song learning in passerine birds and work on social learning of mating preferences. The paper concludes with potential future directions for research on social traditions in systems of courtship behaviour, including determining mechanisms of transmission, genetic and non-social environmental effects, and selective factors influencing the stability of behavioural traditions over time. By integrating proximate and ultimate questions for the transmission of courtship systems, this work would increase our understanding of the ways individual development, cultural processes, and population evolution influence, and are in turn influenced by, one another.     

Critical role of mitochondrial dysfunction and impaired mitophagy in diabetic nephropathy

Mitochondrial dynamics play a critical role in deciding the fate of a cell under normal and diseased condition. Recent surge of studies indicate their regulatory role in meeting energy demands in renal cells making them critical entities in the progression of diabetic nephropathy. Diabetes is remarkably associated with abnormal fuel metabolism, a basis for free radical generation, which if left unchecked may devastate the mitochondria structurally and functionally. Impaired mitochondrial function and their aberrant accumulation have been known to be involved in the manifestation of diabetic nephropathy, indicating perturbed balance of mitochondrial dynamics, and mitochondrial turnover. Mitochondrial dynamics emphasize the critical role of mitochondrial fission proteins such as mitochondrial fission 1, dynamin-related protein 1 and mitochondrial fission factor and fusion proteins including mitofusin-1, mitofusin-2 and optic atrophy 1. Clearance of dysfunctional mitochondria is aided by translocation of autophagy machinery to the impaired mitochondria and subsequent activation of mitophagy regulating proteins PTEN-induced putative kinase 1 and Parkin, for which mitochondrial fission is a prior event. In this review, we discuss recent progression in our understanding of the molecular mechanisms targeting reactive oxygen species mediated alterations in mitochondrial energetics, mitophagy related disorders, impaired glucose transport, tubular atrophy, and renal cell death. The molecular cross talks linking autophagy and renoprotection through an intervention of 5′-AMP-activated protein kinase, mammalian target of rapamycin, and SIRT1 factors are also highlighted here, as in-depth exploration of these pathways may help in deriving therapeutic strategies for managing diabetes provoked end-stage renal disease.