Mechanism of estrogen receptor α inhibiting immune infiltration mediated renal fibrosis following IRI
10.12464/j.issn.1674-7445.2026049
- VernacularTitle:雌激素受体α抑制IRI后免疫浸润介导的肾脏纤维化的机制
- Author:
Mengyuan JIN
1
;
Dawei ZHOU
1
;
Qifa YE
2
Author Information
1. Department of Hepatological Surgery, Central South Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, National Quality Control Center for Donated Organ Procurement, Wuhan 430071, China.
2. Department of Hepatological Surgery, Central South Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, National Quality Control Center for Donated Organ Procurement, Wuhan 430071, China;.
- Publication Type:ReviewArticle
- Keywords:
Estrogen receptor α;
Renal ischemia-reperfusion injury;
Immune infiltration;
Renal fibrosis;
Acute kidney injury;
Chronic kidney disease;
Damage-associated molecular pattern;
Pathogen-associated molecular pattern
- From:
Organ Transplantation
2026;17(5):883-888
- CountryChina
- Language:Chinese
-
Abstract:
Renal ischemia-reperfusion injury (IRI) is an inevitable process in kidney transplantation and certain urological surgeries. IRI causes the release of injury-related molecular patterns by renal tubular epithelial cells, activating innate immune responses and sterile inflammation, leading to the persistence of immune infiltration and tissue remodeling processes, and promoting the transformation of acute kidney injury (AKI) to chronic kidney disease (CKD). CKD is mainly characterized by renal fibrosis, and is associated with the continuous infiltration of immune cells, the release of pro-inflammatory factors and the activation of pro-fibrotic signals. Estrogen receptor (ER) α can regulate the infiltration and activation of immune cells in multiple ways and inhibit renal fibrosis and CKD. This article reviews the specific molecular mechanisms by which ERα regulates immune cell infiltration and inhibits chronic fibrosis after renal IRI, with the aim of providing potential therapeutic targets and scientific basis for future AKI patients.
