Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury.

Biomolecules

Department of Otorhinolaryngology, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai 200031, China.

Published: November 2022


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Ischemia-reperfusion (I/R) injury, uncommon among patients suffering from myocardial infarction, stroke, or acute kidney injury, can result in cell death and organ dysfunction. Previous studies have shown that different types of cell death, including apoptosis, necrosis, and autophagy, can occur during I/R injury. Pyroptosis, which is characterized by cell membrane pore formation, pro-inflammatory cytokine release, and cell burst, and which differentiates itself from apoptosis and necroptosis, has been found to be closely related to I/R injury. Therefore, targeting the signaling pathways and key regulators of pyroptosis may be favorable for the treatment of I/R injury, which is far from adequate at present. This review summarizes the current status of pyroptosis and its connection to I/R in different organs, as well as potential treatment strategies targeting it to combat I/R injury.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687982PMC
http://dx.doi.org/10.3390/biom12111625DOI Listing

Publication Analysis

Top Keywords

i/r injury
20
cell death
8
injury
7
i/r
6
pyroptosis
4
pyroptosis newly
4
newly discovered
4
discovered therapeutic
4
therapeutic target
4
target ischemia-reperfusion
4

Similar Publications

Brazilin, a natural homoisoflavonoid, is the primary bioactive ingredient derived from the bark and heartwood of L. It has been proven to exhibit multiple biological activities and therapeutic potential in chronic degenerative diseases, fibrotic disorders, inflammatory diseases, and cancers. However, whether it is involved in regulating the pathological process of acute kidney injury (AKI) is not fully understood.

View Article and Find Full Text PDF

Numerous people experiencing acute myocardial infarction are also experiencing myocardial ischemia-reperfusion injury (MIRI). Pyroptosis is a core mechanism in MIRI. Tongxinluo (TXL) has a significant protective effect on endothelial cell function.

View Article and Find Full Text PDF

Ethnopharmacological Relevance: Acute kidney injury (AKI) is a growing worldwide health concern. Danggui Shaoyao San (DGSYS) was an frequently-used representative prescription to "promote blood and water and harmonize the body" in traditional Chinese medicine, and its underlying mechanism against AKI remains to be elucidated.

Aim Of The Study: To investigate the protective effect and potential molecular mechanism of DGSYS in alleviating AKI by network pharmacology and experiment validation.

View Article and Find Full Text PDF

Alpinetin protects against myocardial ischemia-reperfusion injury by inhibiting ferroptosis and apoptosis via mitochondrial ferritin.

Eur J Pharmacol

September 2025

Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China. Electronic address:

Purpose: Ischemia-reperfusion injury remains a major problem following myocardial infarction. Alpinetin (ALPT) has been reported to exhibit cardioprotective effects as well as resistance to ischemia-reperfusion injury. However, its role and mechanism during myocardial ischemia-reperfusion injury are unknown.

View Article and Find Full Text PDF

Decreasing H3K27me3 Alleviates Cerebral Ischemia/reperfusion Injury by Modulating FOXP1 Expression.

Free Radic Biol Med

September 2025

Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, Xuzhou, China; National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou China. Electronic address:

Elevated H3K27me3 levels during cerebral I/R injury exacerbate neuronal damage through oxidative stress, but the underlying mechanism remains to be elucidated. We hypothesized that reduced H3K27me3 confers protection by modulating FOXP1 expression. Employing multifaceted approaches, we demonstrate that H3K27me3 reduction in vivo and in vitro enhances lipid metabolism and rescues oxygen-glucose deprivation (OGD)-induced mitochondrial morphological abnormalities and functional deficits.

View Article and Find Full Text PDF