SATB1, senescence and senescence‐related diseases

Author:

Qi Wenjing12,Bai Jinping1,Wang Ruoxi3ORCID,Zeng Xianlu2ORCID,Zhang Lihui1ORCID

Affiliation:

1. Department of Bioscience Changchun Normal University Changchun Jilin China

2. Key Laboratory of Molecular Epigenetics of Ministry of Education, College of Life Sciences Northeast Normal University Changchun Jilin China

3. Center for Cell Structure and Function, College of Life Sciences, Key Laboratory of Animal Resistance Biology of Shandong Province Shandong Normal University Jinan Shandong China

Abstract

AbstractAging leads to an accumulation of cellular mutations and damage, increasing the risk of senescence, apoptosis, and malignant transformation. Cellular senescence, which is pivotal in aging, acts as both a guard against cellular transformation and as a check against cancer progression. It is marked by stable cell cycle arrest, widespread macromolecular changes, a pro‐inflammatory profile, and altered gene expression. However, it remains to be determined whether these differing subsets of senescent cells result from unique intrinsic programs or are influenced by their environmental contexts. Multiple transcription regulators and chromatin modifiers contribute to these alterations. Special AT‐rich sequence‐binding protein 1 (SATB1) stands out as a crucial regulator in this process, orchestrating gene expression by structuring chromatin into loop domains and anchoring DNA elements. This review provides an overview of cellular senescence and delves into the role of SATB1 in senescence‐related diseases. It highlights SATB1's potential in developing antiaging and anticancer strategies, potentially contributing to improved quality of life and addressing aging‐related diseases.

Publisher

Wiley

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