Cellular senescence is a complex program of permanent cell cycle arrest in response to aging, stress or damage leading to the development of hallmark phenotypes such as persistent DNA damage response, metabolic adaptation, apoptosis resistance and a secretory phenotype (the Senescence-Associated Secretory Phenotype, SASP). Recent work has shown that senescence is involved in a variety of endocrine and metabolic disorders such as Type 1 Diabetes, Type 2 Diabetes, monogenic diabetes as well as obesity, fatty liver and cardiovascular disease. However, due to the highly heterogeneous nature of senescence and its cell-type and developmental stage-specificity, there are major gaps in our understanding of: 1) the mechanisms leading to activation of senescence and senescent cell accumulation in the progression of metabolic diseases, 2) the specific markers that accurately distinguish senescent cells from their non-senescent counterparts, and 3) therapeutics that can safely and effectively counteract or mitigate senescent cell accumulation in diabetes and metabolic diseases.
The goals of this research topic are to identify advances in our understanding of how senescence is activated and how senescent cells accumulate and to define specific molecular and phenotypic markers of senescent cells in diabetes and related metabolic diseases. This topic will also highlight innovative therapeutic approaches to mitigating senescent cells and their deleterious effects in diabetes and metabolic diseases.
The scope of this topic is Primary Research Articles and Reviews that align with the criteria below:
• Studies that identify/define mechanisms of senescent cell generation, accumulation or turnover in diabetes or related metabolic diseases
• Studies that characterize novel senescent cell markers and/or phenotypes in models of diabetes
• Studies that test or characterize novel anti-senescence therapeutics in animal or human models of diabetes and metabolic diseases
• Review articles that summarize, mechanistic knowledge, current trends or highlight existing knowledge gaps and future directions for the study of senescence in diabetes and metabolic diseases
Cellular senescence is a complex program of permanent cell cycle arrest in response to aging, stress or damage leading to the development of hallmark phenotypes such as persistent DNA damage response, metabolic adaptation, apoptosis resistance and a secretory phenotype (the Senescence-Associated Secretory Phenotype, SASP). Recent work has shown that senescence is involved in a variety of endocrine and metabolic disorders such as Type 1 Diabetes, Type 2 Diabetes, monogenic diabetes as well as obesity, fatty liver and cardiovascular disease. However, due to the highly heterogeneous nature of senescence and its cell-type and developmental stage-specificity, there are major gaps in our understanding of: 1) the mechanisms leading to activation of senescence and senescent cell accumulation in the progression of metabolic diseases, 2) the specific markers that accurately distinguish senescent cells from their non-senescent counterparts, and 3) therapeutics that can safely and effectively counteract or mitigate senescent cell accumulation in diabetes and metabolic diseases.
The goals of this research topic are to identify advances in our understanding of how senescence is activated and how senescent cells accumulate and to define specific molecular and phenotypic markers of senescent cells in diabetes and related metabolic diseases. This topic will also highlight innovative therapeutic approaches to mitigating senescent cells and their deleterious effects in diabetes and metabolic diseases.
The scope of this topic is Primary Research Articles and Reviews that align with the criteria below:
• Studies that identify/define mechanisms of senescent cell generation, accumulation or turnover in diabetes or related metabolic diseases
• Studies that characterize novel senescent cell markers and/or phenotypes in models of diabetes
• Studies that test or characterize novel anti-senescence therapeutics in animal or human models of diabetes and metabolic diseases
• Review articles that summarize, mechanistic knowledge, current trends or highlight existing knowledge gaps and future directions for the study of senescence in diabetes and metabolic diseases
