The exosome of MSCs derived from human umbilical cord blood (HUCB-MSC) has been reported to have cardioprotective effects on mouse models of acute myocardial infarction (AMI) and cardiomyocyte hypoxia injury, but the exact mechanisms involved require further investigation. This paper aimed to study the role of HUCB-MSC-exosomes in inhibiting ferroptosis to attenuate myocardial injury. Compared with sham or normoxia groups, RT-PCR and western blotting showed that divalent metal transporter 1 (DMT1) expression was significantly increased, and Prussian blue staining, ferrous iron (Fe), MDA, and GSH level detection demonstrated that ferroptosis occurred in the infraction myocardium and in cardiomyocyte following hypoxia-induced injury. Overexpression of DMT1 promoted H/R-induced myocardial cell ferroptosis, while knockdown of DMT1 significantly inhibited the ferroptosis. HUCB-MSCs-derived exosomes inhibited ferroptosis and reduced myocardial injury, which was abolished in exosome with miR-23a-3p knockout. Moreover, dual luciferase reporter assay confirmed that DMT1 was a target gene of miR-23a-3p. In conclusion, HUCB-MSCs-exosomes may suppress DMT1 expression by miR-23a-3p to inhibit ferroptosis and attenuate myocardial injury.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10565-020-09530-8 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
β2-Adrenergic Receptor Agonist Clenbuterol Protects Against Acute Ischemia/Reperfusion-Induced Arrhythmia by Regulation of Akt/eNOS/NO/Cx43 Signaling Pathway.
Pharmacol Res Perspect
February 2025
Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ventricular arrhythmias induced by ischemia/reperfusion injury limits the therapeutic effect of early reperfusion therapy for acute myocardial infarction. This study investigated the protective effects of the β2-adrenergic receptor (β2-AR) agonist clenbuterol against ischemia/reperfusion-induced arrhythmias and the underlying mechanism. Anesthetized rats were subjected to 10-min left coronary artery occlusion and 10-min reperfusion in vivo.
View Article and Find Full Text PDFMitigating PM Induced Myocardial Metal Deposition Through Sodium Thiosulfate Resulted in Reduction of Cardiotoxicity and Physiological Recovery From Ischemia-Reperfusion via Mitochondrial Preservation.
Environ Toxicol
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
The cardiovascular risks linked to PM include calcification in both vasculature and myocardial tissues, leading to structural changes and functional decline. Through the selection of a clinically proven endogenous agent, sodium thiosulfate (STS), capable of addressing PM related cardiac abnormalities, we not only address the absence of effective solutions to mitigate PM toxicity, but also provide evidence for the repurposing potential of STS in ameliorating PM induced cardiac damage. Female Wistar rats were exposed to PM (250 μg/m) for 3 h daily for 21 days.
View Article and Find Full Text PDFSuccessful management of coagulation dysfunction in a patient with fulminant myocarditis: a case report.
Front Cardiovasc Med
January 2025
Department of Clinical Laboratory, Wuhan Asia Heart Hospital, Wuhan, China.
Fulminant myocarditis (FM) is an acute, diffuse inflammatory myocardial disease characterized by abrupt onset and extremely rapid progression. Patients typically exhibit haemodynamic abnormalities that may lead to respiratory failure, liver and renal failure, and subsequent coagulopathy. Collectively, these complications significantly increase the risk of early mortality.
View Article and Find Full Text PDFMitochondrial transplantation for the treatment of cardiac and noncardiac diseases: mechanisms, prospective, and challenges.
Life Med
April 2024
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Mitochondrial transplantation (MT) is a promising therapeutic strategy that involves introducing healthy mitochondria into damaged tissues to restore cellular function. This approach has shown promise in treating cardiac diseases, such as ischemia-reperfusion injury, myocardial infarction, and heart failure, where mitochondrial dysfunction plays a crucial role. Transplanting healthy mitochondria into affected cardiac tissue has resulted in improved cardiac function, reduced infract size, and enhanced cell survival in preclinical studies.
View Article and Find Full Text PDFManagement of Patients with Myocardial Injury After Noncardiac Surgery: A Retrospective Chart Review.
CJC Open
January 2025
Population Health Research Institute, McMaster University, Hamilton, Ontario, Canada.
Background: Myocardial injury after noncardiac surgery (MINS) is associated with an increased incidence of cardiac morbidity and mortality. Little is known about how these patients are managed.
Methods: We performed a single-centre retrospective chart review of patients referred to a postoperative clinic with the diagnosis of MINS.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!