The growing burden of metabolic diseases has hastened the search for governing biological processes. Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. It is defined as a state of irreversible cell cycle arrest induced by different stressors, such as DNA damage, telomere shortening, radiation, oxidative stress, mitochondrial dysfunction, mitogenic and metabolic stressors. Senescent cells often develops a senescence-associated secretory phenotype (SASP) to prompt immune clearance, which derives chronic sterile inflammation and plays a casual role in the development and progression of metabolic diseases such as obesity and diabetes. Diabetes-induced senescence would further promote chronic inflammation and initiate a vicious cycle of senescent cell formation in multiple tissues. Thus, senescent cells might be part of a pathogenic loop, as both a cause and consequence of metabolic changes and tissue damage. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and suppressing certain modules of the SASP (senomorphics). However, our current understanding of senotherapy is not yet complete. More research is therefore needed to understand the kinetics of senescent cell formation, especially in the setting of persisting metabolic stimuli, and also to define the advantages of senolytics when compared to current therapies for metabolic disorders.
The aim of this Special Issue is to solicit original research, review and mini-review articles that illustrate or comment on the mechanisms underlying the pathogenesis of metabolic diseases with a focus on the senescent phenotypes of cells, and could support the development of therapeutic strategies.
Potential topics include but are not limited to the following:
• Identification of molecular mechanisms of senescence in metabolic diseases.
• Regulation and function of SASP.
• Animal models to study senescence in metabolic diseases.
• Identification of senolytic or senomorphic compounds and their mechanism of action.
• Invitro studies on the effects of senolytics or senomorphics on specific cell population.
The growing burden of metabolic diseases has hastened the search for governing biological processes. Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. It is defined as a state of irreversible cell cycle arrest induced by different stressors, such as DNA damage, telomere shortening, radiation, oxidative stress, mitochondrial dysfunction, mitogenic and metabolic stressors. Senescent cells often develops a senescence-associated secretory phenotype (SASP) to prompt immune clearance, which derives chronic sterile inflammation and plays a casual role in the development and progression of metabolic diseases such as obesity and diabetes. Diabetes-induced senescence would further promote chronic inflammation and initiate a vicious cycle of senescent cell formation in multiple tissues. Thus, senescent cells might be part of a pathogenic loop, as both a cause and consequence of metabolic changes and tissue damage. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and suppressing certain modules of the SASP (senomorphics). However, our current understanding of senotherapy is not yet complete. More research is therefore needed to understand the kinetics of senescent cell formation, especially in the setting of persisting metabolic stimuli, and also to define the advantages of senolytics when compared to current therapies for metabolic disorders.
The aim of this Special Issue is to solicit original research, review and mini-review articles that illustrate or comment on the mechanisms underlying the pathogenesis of metabolic diseases with a focus on the senescent phenotypes of cells, and could support the development of therapeutic strategies.
Potential topics include but are not limited to the following:
• Identification of molecular mechanisms of senescence in metabolic diseases.
• Regulation and function of SASP.
• Animal models to study senescence in metabolic diseases.
• Identification of senolytic or senomorphic compounds and their mechanism of action.
• Invitro studies on the effects of senolytics or senomorphics on specific cell population.
