Since the discovery about shared signaling pathways that extend lifespan in organisms, ranging from yeast to nematodes to fruit flies to mammals, a great deal of attention has been devoted to understanding aging as a generalized phenomenon, and to unraveling the genetics of these pathways and mechanisms that control it. However, demographic data on large numbers of diverse species actually show that aging is far from universal. Furthermore, among species that do age, lifespans can differ more than 1000-fold, and the underlying mechanisms, genetics, and patterns can be remarkably variable. Attempts to translate knowledge of the basic biology of aging into biomedical and clinical contexts thus require an understanding of not only what is shared, but also what is not shared. For example, even if a certain conserved pathway is present in humans, its impact may be more limited in humans than other species, or it may interact with a human-specific mechanism.
In this context, it is crucial to deepen our understanding of how specific pathways and cellular/molecular mechanisms contribute to the demographic and evolutionary diversity of aging patterns across the tree of life. How are the known conserved signaling pathways contributing to aging (e.g. insulin/IGF-1 and mTOR signaling) used in species that do not age? Do slowly aging species repeatedly evolve the same strategies, or do they each evolve unique ones? How broadly are mechanisms such as inflammation or mitochondrial dysfunction distributed across the tree of life? The answers to these questions may often require going beyond standard model organisms, which have generally been chosen because of their fast aging rates within their clades. Moreover, they may require detailed studies of (1) mechanisms within outlier species, (2) genetic control of evolutionary diversity of the aging process, and (3) comparative studies incorporating genetic or molecular data. A mechanistic understanding of aging has also been little explored in plants and bacteria, and there is therefore a need to broaden the taxonomic scope of our understanding of mechanisms of aging.
In this Research Topic, we welcome all articles types that shed light on the diversity of aging across species based on cellular/molecular mechanisms or pathways. We also welcome studies that highlight the importance of this perspective for applications to humans.
In particular, we aim to cover the following points:
• Understanding the conserved signaling pathways contributing to aging in non-aging species, such as hydra.
• Genetic or mechanistic variation determining lifespan within taxa (e.g. IGF-1 levels in mammals).
• Studies of aging mechanisms and pathways in understudied taxa (e.g. plants, bacteria, mollusks, colonial invertebrates, marsupials).
• Genomic variation in relation to aging demography or mechanisms.
• Delimiting the taxonomic breadth of known aging mechanisms.
• Mechanisms of aging avoidance in long-lived and non-aging species.
• Clinical or epidemiological studies demonstrating the importance of human- or primate-specific mechanisms of aging.
Since the discovery about shared signaling pathways that extend lifespan in organisms, ranging from yeast to nematodes to fruit flies to mammals, a great deal of attention has been devoted to understanding aging as a generalized phenomenon, and to unraveling the genetics of these pathways and mechanisms that control it. However, demographic data on large numbers of diverse species actually show that aging is far from universal. Furthermore, among species that do age, lifespans can differ more than 1000-fold, and the underlying mechanisms, genetics, and patterns can be remarkably variable. Attempts to translate knowledge of the basic biology of aging into biomedical and clinical contexts thus require an understanding of not only what is shared, but also what is not shared. For example, even if a certain conserved pathway is present in humans, its impact may be more limited in humans than other species, or it may interact with a human-specific mechanism.
In this context, it is crucial to deepen our understanding of how specific pathways and cellular/molecular mechanisms contribute to the demographic and evolutionary diversity of aging patterns across the tree of life. How are the known conserved signaling pathways contributing to aging (e.g. insulin/IGF-1 and mTOR signaling) used in species that do not age? Do slowly aging species repeatedly evolve the same strategies, or do they each evolve unique ones? How broadly are mechanisms such as inflammation or mitochondrial dysfunction distributed across the tree of life? The answers to these questions may often require going beyond standard model organisms, which have generally been chosen because of their fast aging rates within their clades. Moreover, they may require detailed studies of (1) mechanisms within outlier species, (2) genetic control of evolutionary diversity of the aging process, and (3) comparative studies incorporating genetic or molecular data. A mechanistic understanding of aging has also been little explored in plants and bacteria, and there is therefore a need to broaden the taxonomic scope of our understanding of mechanisms of aging.
In this Research Topic, we welcome all articles types that shed light on the diversity of aging across species based on cellular/molecular mechanisms or pathways. We also welcome studies that highlight the importance of this perspective for applications to humans.
In particular, we aim to cover the following points:
• Understanding the conserved signaling pathways contributing to aging in non-aging species, such as hydra.
• Genetic or mechanistic variation determining lifespan within taxa (e.g. IGF-1 levels in mammals).
• Studies of aging mechanisms and pathways in understudied taxa (e.g. plants, bacteria, mollusks, colonial invertebrates, marsupials).
• Genomic variation in relation to aging demography or mechanisms.
• Delimiting the taxonomic breadth of known aging mechanisms.
• Mechanisms of aging avoidance in long-lived and non-aging species.
• Clinical or epidemiological studies demonstrating the importance of human- or primate-specific mechanisms of aging.
