Peroxisome proliferator activated receptor-α in renal injury: mechanisms and therapeutic implications.
10.3760/cma.j.cn121430-20250318-00270
- Author:
Jing ZHOU
1
;
Li LUO
;
Junyu ZHU
;
Huaping LIANG
;
Shengxiang AO
Author Information
1. Department of Wound Infection and Special Drugs Research, Daping Hospital, Army Medical University, State Key Laboratory of Trauma and Chemical Poisoning, Chongqing 400042, China. Corresponding author: Ao Shengxiang, Email: sanyida2008@sina.com.
- Publication Type:English Abstract
- MeSH:
Humans;
PPAR alpha/metabolism*;
Acute Kidney Injury/therapy*;
Animals;
Kidney/metabolism*
- From:
Chinese Critical Care Medicine
2025;37(7):693-697
- CountryChina
- Language:Chinese
-
Abstract:
Peroxisome proliferator activated receptor-α (PPAR-α) is significantly expressed in various tissues such as the liver, kidney, myocardium, and skeletal muscle, which plays a central role in the development of various diseases by regulating key physiological processes such as energy homeostasis, redox balance, inflammatory response, and ferroptosis. As an important metabolic and excretory organ of the body, renal dysfunction can lead to water and electrolyte imbalance, toxin accumulation, and multiple system complications. The causes of kidney injury are complex and diverse, including acute injury factors (such as ischemia/reperfusion, nephrotoxic drugs, septic shock, and immune glomerulopathy), as well as chronic progressive causes [such as metabolic disease-related nephropathy, hypertensive nephropathy (HN)], and risk factors such as alcohol abuse, obesity, and aging. This review briefly describes the structure, function, and activity regulation mechanism of PPAR-α, systematically elucidates the molecular regulatory network of PPAR-α in the pathological process of kidney injury including acute kidney injury (AKI) such as renal ischemia/reperfusion injury (IRI), drug-induced AKI, sepsis-associated acute kidney injury (SA-AKI), glomerulonephritis, chronic kidney disease (CKD) such as diabetic nephropathy (DN), HN, and other kidney injury, and summarizes the mechanisms related to PPAR-α regulation of kidney injury, including regulation of metabolism, antioxidation, anti-inflammation, anti-fibrosis, and anti-ferroptosis. This review also evaluates PPAR-α's medical value as a novel therapeutic target, and aims to provide theoretical basis for the development of kidney protection strategies based on PPAR-α targeted intervention.
