Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

The present review describes the mechanisms of NETosis and its role in myocardial ischemia-reperfusion injury (MIRI), focusing on the release of neutrophil extracellular traps (NETs) by activated neutrophils. NETs, composed of depolymerized chromatin and granule proteins, are crucial for pathogen entrapment, infection control and immune regulation. However, NET formation, linked to neutrophil death (NETosis), exacerbates MIRI by promoting inflammation and tissue damage. To address therapeutic strategies for NETosis in MIRI, several potential clinically significant approaches were explored, including peptidylarginine deaminase 4 inhibition, DNase therapy, antioxidants, inflammation modulation, and antithrombotic treatments, which not only provide novel diagnostic biomarkers and therapeutic targets in MIRI, but are also expected to improve patient prognosis and advance the development of personalised medicine.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105085PMC
http://dx.doi.org/10.3892/br.2025.1991DOI Listing

Publication Analysis

Top Keywords

myocardial ischemia-reperfusion
8
ischemia-reperfusion injury
8
netosis
4
netosis myocardial
4
injury mechanisms
4
mechanisms therapies
4
therapies review
4
review review
4
review describes
4
describes mechanisms
4

Similar Publications

Myocardial ischemia-reperfusion injury (MIRI) endures as a substantial impediment to the management of cardiovascular disease. The pathophysiology of MIRI is complex, involving oxidative stress, calcium overload, inflammation, and apoptosis. The NRG1/ErbB4 signaling pathway has been implicated in modulating oxidative stress responses in the heart, potentially reducing cellular damage caused by free radicals.

View Article and Find Full Text PDF

Hypoxia Aggravates Myocardial Ischemia/Reperfusion Injury Through the Promotion of Ferroptosis via ACSL4 Lactylation.

J Cardiovasc Transl Res

September 2025

Department of Cardiology, Bei'an Hospital, Beidahuang Group, Heihe, 164000, Heilongjiang Province, China.

Myocardial ischemia/reperfusion injury (MIRI) worsens ischemic damage, with ferroptosis as a key mediator of this iron-dependent cell death. Lactylation, a novel epigenetic modification, remains poorly understood in MIRI-associated ferroptosis. This study aimed to elucidate the mechanistic link between lactylation and ferroptosis in MIRI.

View Article and Find Full Text PDF

Gap junctions (GJs) are critical structures for cardiac electrical signal conduction and synchronized contraction. Their fundamental components are transmembrane proteins from the connexin (Cx) family, which assemble into hexameric channels to form intercellular ion-permeable pathways, ensuring efficient electrical transmission and coordinated contraction between cardiac cells. Connexin 43 (Cx43), the most abundant connexin in the heart, serves as the primary constituent of ventricular gap junctions.

View Article and Find Full Text PDF

Objective: This study aims to investigate the potential of electroacupuncture to mitigate myocardial ischemia-reperfusion injury (MIRI) by influencing N6-methyladenosine (m6A) methylation through modulation of the fat mass and obesity-associated protein (FTO).

Methods: An experimental murine model of MIRI was established by surgically occluding the left anterior descending coronary artery, followed by reperfusion. Electroacupuncture treatment targeting Neiguan acupoints was administered 7 days before ischemia induction.

View Article and Find Full Text PDF

Chrysin Attenuates Myocardial Cell Apoptosis in Mice.

Cardiovasc Toxicol

September 2025

Department of Cardiac Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Cardiovascular Institute, Guangzhou, 510100, Guangdong, China.

Myocardial infarction (MI), induced by ischemia and hypoxia of the coronary arteries, presents as myocardial necrosis. Patients often experience intense, prolonged retrosternal pain that is unrelieved by rest or nitrate therapy and is frequently associated with high blood myocardial enzyme levels. Physical effort may exacerbate this anxiety, increasing the likelihood of life-threatening consequences such as arrhythmias, shock, or cardiac failure.

View Article and Find Full Text PDF