Extracellular vesicles (EVs) are small-sized membrane-surrounded structures released from cells into the blood, which play important roles in regulating various biological processes. However, the role of EVs in Doxorubicin (DOX)-induced cardiomyocytes senescence remains elusive. In this study, we found that human serum EVs inhibited DOX-induced senescence in H9C2 cells, which was abolished by miR-34a mimic. Our study also proved that miR-34a mediated DOX-induced H9C2 cell senescence by targeting phosphatase 1 nuclear targeting subunit (PNUTS). In addition to the downregulation of miR-34a, EVs could upregulate the expression of PNUTS. Moreover, the inhibitory effect of serum EVs on DOX-induced H9C2 cell senescence was also impeded by PNUTS siRNA. In conclusion, our study suggests that serum EVs retard H9C2 cell senescence through the miR-34a/PNUTS pathway, providing a potential therapy for cardiac aging.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s12265-018-9847-4 | DOI Listing |
Ecotoxicol Environ Saf
January 2025
Department of Cardiology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 1 Minde Road, Nanchang, Jiangxi Province 330006, China. Electronic address:
Aims: Nanoplastics (NPs) are emerging organic pollutants generated by plastic degradation and are ubiquitous in the environment. They can be accumulated through the food webs and enter the human body through dietary intake, posing health risks. The main target organs of NP accumulation are the lungs, liver, heart, and kidneys.
View Article and Find Full Text PDFJ Cardiothorac Surg
January 2025
The First Hospital of Lanzhou University, Lanzhou, China.
Background: This article aims to use high-throughput sequencing to identify miRNAs associated with ferroptosis in myocardial ischemia-reperfusion injury, select a target miRNA, and investigate its role in H9C2 cells hypoxia-reoxygenation injury.
Methods: SD rats and H9C2 cells were used as subjects. ELISA kits quantified MDA, SOD, GSH, LDH, and ferritin levels.
Medicine (Baltimore)
November 2024
Yantai Yuhuangding Hospital, Shandong, China.
Background: The neutrophil-mediated generation of neutrophil extracellular traps (NETs) results in an augmented inflammatory response and cellular tissue injury during acute myocardial infarction (AMI). Through the analysis of public database information, we discovered and confirmed putative critical genes involved in NETs-mediated AMI.
Methods: The AMI dataset GSE66360 and the single-cell dataset GSE163465 were downloaded from the Gene Expression Omnibus database.
Appl Biochem Biotechnol
January 2025
Department of Internal Medicine-Cardiovascular, Guangzhou Twelfth People's Hospital, No.1, Tianqiang Road, Tianhe District, Guangzhou City, Guangdong Province, 510620, China.
Myocardial infarction (MI) is a coronary artery-related disease that seriously threatens human life and is the leading cause of sudden death worldwide, where a lack of nutrients and oxygen leads to an inflammatory response and death of cardiomyocytes. Ferroptosis is a form of non-apoptotic cell death associated with metabolic dysfunction, resulting in abnormal breakdown of glutamine and iron-dependent accumulation of reactive oxygen species (ROS) during metabolism. However, the molecular mechanism of ferroptosis in the pathogenesis of MI and the function of Klotho and KRAS on ferroptosis during MI remain unclear.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address:
Chronic ethanol (EtOH) consumption has been widely recognized as a significant contributor to cardiotoxicity. However, no specific treatment is currently available to ameliorate chronic ethanol induced cardiotoxicity. Adiponectin receptor agonist AdipoRon exerts protective effects in multiple organs through alleviating lipotoxicity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!