SATB1, senescence and senescence-related diseases

J Cell Physiol. 2024 Aug;239(8):e31327. doi: 10.1002/jcp.31327. Epub 2024 May 27.

Abstract

Aging 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.

Keywords: SATB1; aging‐related diseases; cellular senescence; immunosenescence; neurodegeneration.

Publication types

  • Review

MeSH terms

  • Aging / genetics
  • Aging / metabolism
  • Aging / pathology
  • Animals
  • Cellular Senescence* / genetics
  • Chromatin / genetics
  • Chromatin / metabolism
  • Humans
  • Matrix Attachment Region Binding Proteins* / genetics
  • Matrix Attachment Region Binding Proteins* / metabolism
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Neoplasms / pathology

Substances

  • Matrix Attachment Region Binding Proteins
  • SATB1 protein, human
  • Chromatin