Year: 2025
Type: editorial
Abstract: Phenotype (SASP) (Campisi and d'Adda di 2007). A key driver of celular senesence is the progressive shortening of telomeres that occurs with aging. Additionally, cells can enter senescence in response to various stressprs, including sustained mitogenic signaling, oncogene activation, DNA damage from irradiation, oxidative and genotoxic stress, epigenetic alterations, chromatin disorganization, perturbed proteostasis, mitochondrial dysfunction, inflammation signals, tissue damage, chemotherapeutic agents, and nutrient deprivation (Kumari and Jat, 2021).Both cellular senescence and organismal aging are closely conected to epigenetic states.During development, epigenetic modifications, including DNA methylation, histone modifications, and chromatin remodeling, collectively determine cellular differentiation status and cell fates. These differentiation states can also be reversed through the transcriptional and/or epigentic reprogramming of the cell. In cell reprogramming, the cell identity and plasticity can be altered by the overexpression of transcription factors such as Oct4, Sox2, Klf4 and c-Myc (OSKM) (Takahashi and Yamanaka, 2006). This induction creates a dedifferentiation state that enhances tissue regeneration and has been succesfully applied in various pathological contexts, including diabetes, muscle injuries, retinal degeneration, and myocardial infartion (Ocampo et al., 2016;Lu et al., 2020;Chen et al., 2021). Those We hope that the articles featured in this research topic will serve as valuable resources for researchers in the fields of aging, senescence, and cell reprogramming, whether they are well-established experts or newcomers eager to explore this exciting arena.
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W4410450441