EDITORIAL article
Front. Cell Dev. Biol.
Sec. Stem Cell Research
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1622682
This article is part of the Research TopicSenescence and Reprogramming: Hallmarks in Aging and DiseaseView all 6 articles
Editorial: Senescence and Reprogramming: Hallmarks in Aging and Disease
Provisionally accepted
- 1University of Extremadura, Badajoz, Spain
- 2Washington State University Health Sciences Spokane, Spokane, United States
- 3Department of Otolaryngology-Head and Neck Surgery, Washington University School of Medicine, Saint Louis, MO 63110, USA, St. Louis, United States
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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.
Keywords: reprogramming, Aging, senescence, OSKM, Cancer, transdifferentiation, progeroid syndromes
Received: 04 May 2025; Accepted: 05 May 2025.
Copyright: © 2025 González Rico, Zhu and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: F Javier González Rico, University of Extremadura, Badajoz, Spain
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