Cellular senescence, first discovered by Hayflick and Moorhead in 1961, is a cellular response to extrinsic stressors and exhaustion of rate-limiting replication characterized by permanent cell cycle arrest. Among the extrinsic stressors that lead to senescence induction, there are various factors such as oncogene activation, oxidative stress, DNA damage, treatment with chemotherapeutics. Although senescent cells have lost their ability to proliferate, they are metabolically and transcriptionally active cells. One of their most distinctive features is the ability to communicate with the cells in their microenvironment by secreting numerous senescence-related secretory phenotype (SASP) factors, including inflammatory cytokines, chemokines, growth factors, and metalloproteinases.
Senescent cells accumulate in various tissues with aging, and preventing this accumulation delays age-related pathologies, such as idiopathic pulmonary fibrosis, obesity, Type 2 diabetes, cataract and sarcopenia. Senescent cells also have pro-tumorigenic activities, such as inducing epithelial-mesenchymal transition (EMT) and promoting tumor vascularization. Treatment with chemotherapeutics also induces cellular senescence in normal and cancer cells causing SASP secretion. It has been determined that chemotherapeutics-induced SASP enhances tumor growth in surrounding cells and leads to the development of resistance to chemotherapeutic drugs.
The accumulating evidence has shown that cellular senescence plays an important role in different physiological and pathological processes. Taken together, determining the roles of cellular senescence in physiological and pathophysiological processes is important both for a better understanding of pathological processes and for developing new treatment strategies targeting the senescent cell.
The goal of this Research Topic is to further elucidate the physiological and pathophysiological processes involving cellular senescence.
Authors should focus on the following, but not limited to: as embryonic development, tissue homeostasis and tissue repair, wound healing, and the ability to limit tumor progression by ensuring that the genomes of potentially dysfunctional, damaged, or transformed cells are not passed on to the next generation, senomorphic and senolytic drug discovery.
Topic Editor Dr. Mohammad Nasir Uddin is the founder and CEO of Emergent Biotechnologies, LLC. The other Topic Editors declare no competing interests with regard to the Research Topic subject.Cellular senescence, first discovered by Hayflick and Moorhead in 1961, is a cellular response to extrinsic stressors and exhaustion of rate-limiting replication characterized by permanent cell cycle arrest. Among the extrinsic stressors that lead to senescence induction, there are various factors such as oncogene activation, oxidative stress, DNA damage, treatment with chemotherapeutics. Although senescent cells have lost their ability to proliferate, they are metabolically and transcriptionally active cells. One of their most distinctive features is the ability to communicate with the cells in their microenvironment by secreting numerous senescence-related secretory phenotype (SASP) factors, including inflammatory cytokines, chemokines, growth factors, and metalloproteinases.
Senescent cells accumulate in various tissues with aging, and preventing this accumulation delays age-related pathologies, such as idiopathic pulmonary fibrosis, obesity, Type 2 diabetes, cataract and sarcopenia. Senescent cells also have pro-tumorigenic activities, such as inducing epithelial-mesenchymal transition (EMT) and promoting tumor vascularization. Treatment with chemotherapeutics also induces cellular senescence in normal and cancer cells causing SASP secretion. It has been determined that chemotherapeutics-induced SASP enhances tumor growth in surrounding cells and leads to the development of resistance to chemotherapeutic drugs.
The accumulating evidence has shown that cellular senescence plays an important role in different physiological and pathological processes. Taken together, determining the roles of cellular senescence in physiological and pathophysiological processes is important both for a better understanding of pathological processes and for developing new treatment strategies targeting the senescent cell.
The goal of this Research Topic is to further elucidate the physiological and pathophysiological processes involving cellular senescence.
Authors should focus on the following, but not limited to: as embryonic development, tissue homeostasis and tissue repair, wound healing, and the ability to limit tumor progression by ensuring that the genomes of potentially dysfunctional, damaged, or transformed cells are not passed on to the next generation, senomorphic and senolytic drug discovery.
Topic Editor Dr. Mohammad Nasir Uddin is the founder and CEO of Emergent Biotechnologies, LLC. The other Topic Editors declare no competing interests with regard to the Research Topic subject.