SATB1, senescence and senescence-related diseases.
Wenjing QiJinping BaiRuoxi WangXianlu ZengLihui ZhangPublished in: Journal of cellular physiology (2024)
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.
Keyphrases
- cell cycle arrest
- dna damage
- gene expression
- endothelial cells
- cell death
- transcription factor
- stress induced
- oxidative stress
- pi k akt
- dna methylation
- binding protein
- public health
- genome wide
- squamous cell carcinoma
- cell proliferation
- endoplasmic reticulum stress
- human health
- risk assessment
- drug induced
- young adults
- climate change
- lymph node metastasis
- amino acid