Role of m6A RNA methylation in renal resident cell injury.
10.11817/j.issn.1672-7347.2024.230600
- Author:
Zixia ZHAO
1
,
2
;
Chen ZHANG
3
;
Si WU
3
;
Junjun LUAN
3
;
Hua ZHOU
2
,
4
Author Information
1. Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang 110000, China. zhaozixia_cmu@
2. com.
3. Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang 110000, China.
4. Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang 110000, China. huazhou_cmu@
- Publication Type:Review
- Keywords:
N 6-methyladenosine;
RNA methylation;
acute kidney injury;
chronic kidney disease;
renal resident cell
- MeSH:
Humans;
Methylation;
Adenosine/metabolism*;
Methyltransferases/metabolism*;
Kidney/metabolism*;
Kidney Diseases/pathology*;
Epigenesis, Genetic;
RNA/genetics*;
RNA Methylation
- From:
Journal of Central South University(Medical Sciences)
2024;49(11):1757-1768
- CountryChina
- Language:English
-
Abstract:
RNA methylation modification is a highly dynamic and reversible epigenetic regulatory mechanism, primarily controlled by 3 types of factors: Methyltransferases, demethylases, and methylation reader proteins. N6-methyladenosine (m6A) methylation is the most common form of RNA methylation, and dysregulation of this process may lead to the development of various diseases. Renal diseases have drawn considerable attention owing to their high incidence, poor prognosis, and substantial socioeconomic burden. Renal resident cell injury plays a crucial role in the onset and progression of various kidney diseases. Understanding the mechanisms underlying renal resident cell injury is essential for advancing the prevention and treatment of kidney diseases. Recent studies have revealed that RNA m6A methylation plays a critical role in renal resident cell injury, highlighting its potential as a novel therapeutic target for kidney disease treatment.
