Adipose ZFP36 protects against diet-induced obesity and insulin resistance.

Aims: Obesity, as a worldwide healthcare problem, has become more prevalent. ZFP36 is a well-known RNA-binding protein and involved in the posttranscriptional regulation of many physiological processes. Whether the adipose ZFP36 plays a role in obesity and insulin resistance remains unclear.

FBLN7 mediates vascular smooth muscle cell phenotype switching and vascular remodeling in hypertension.

Arterial remodeling serves as a pivotal mechanism underlying the development of diseases such as hypertension. Fibulin-7 (FBLN7), an adhesion protein, remains enigmatic regarding its role in these pathological processes. This study aims to explore whether FBLN7 influences vascular remodeling and its underlying mechanisms.

Retraction Notice to: miR-146a inhibits mitochondrial dysfunction and myocardial infarction by targeting cyclophilin D.

[This retracts the article DOI: 10.1016/j.omtn.

Retraction Notice to: MicroRNA-494 Inhibits the LRG1 Expression to Induce Proliferation and Migration of VECs in Rats following Myocardial Infarction.

[This retracts the article DOI: 10.1016/j.omtn.

Effects of resveratrol supplementation on cardiac remodeling in hypertensive patients: a randomized controlled clinical trial.

Resveratrol (RES) has been demonstrated to be protective in the cardiovascular system in animal studies, but the evidence is limited in humans. The purpose of the study was to evaluate the effect of RES supplementation on cardiac remodeling in patients with hypertension. Eighty Subjects were randomly divided into RES group (plus RES 400 mg/d in addition to conventional therapy, n = 43) and control group (conventional therapy, n = 37).

MicroRNA-136-5p protects cardiomyocytes from coronary microembolization through the inhibition of pyroptosis.

This study investigated how miR-136-5p partially affected cardiomyocyte pyroptosis in rats with coronary microembolization (CME). The cardiac function and structure of rats with CME were evaluated using echocardiography, hematoxylin and eosin staining, Masson staining, and troponin I level. Pyroptosis was induced by lipopolysaccharide (LPS) in isolated rat cardiomyocytes and evaluated by the expression of caspase-1, NOD-like receptor family pyrin domain-containing 3, interleukin-1β, and gasdermin D-N.

Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.

In this study, we aim to investigate the regulation of specific long non-coding RNAs (lncRNAs) on the progression of ischemia/reperfusion (I/R) injury. We identified and characterized the exosomes derived from mouse primary aortic endothelial cells. Subsequently, we found that these exosomes expressed typical exosomal markers and high levels of LINC00174, which significantly ameliorated I/R-induced myocardial damage and suppressed the apoptosis, vacuolation, and autophagy of myocardial cells.

miR-146a inhibits mitochondrial dysfunction and myocardial infarction by targeting cyclophilin D.

Increasing evidence suggests that mitochondrial microRNAs (miRNAs) are implicated in the pathogenesis of cardiovascular diseases; however, their roles in ischemic heart disease remain unclear. Herein, we demonstrate that miR-146a is enriched in the mitochondrial fraction of cardiomyocytes, and its level significantly decreases after ischemic reperfusion (I/R) challenge. Cardiomyocyte-specific knockout of miR-146a aggravated myocardial infarction, apoptosis, and cardiac dysfunction induced by the I/R injury.

Alprostadil Injection Attenuates Coronary Microembolization-Induced Myocardial Injury Through GSK-3β/Nrf2/HO-1 Signaling-Mediated Apoptosis Inhibition.

Objective: Coronary microembolization (CME) results in progressive contractile dysfunction associated with cardiomyocyte apoptosis. Alprostadil injection improves microcirculation, which is effective in treating various cardiovascular disorders. However, the therapeutic effects of alprostadil in CME-induced myocardia injury remain unknown.

Long non-coding RNA CASC7 is associated with the pathogenesis of heart failure via modulating the expression of miR-30c.

MiRNAs can be used as promising diagnostic biomarkers of heart failure, while lncRNAs act as competing endogenous RNAs of miRNAs. In this study, we collected peripheral blood monocytes from subjects with or without HF to explore the association between certain lncRNAs, miRNAs and HF. Heart failure patients with preserved or reduced ejection fraction were recruited for investigation.

LncRNA TUG1 mediates ischemic myocardial injury by targeting miR-132-3p/HDAC3 axis.

Increased production of reactive oxygen species (ROS) significantly contributed to the pathogenesis of acute myocardial infarction (AMI). Recent studies suggest that hypoxia upregulated the long noncoding RNA taurine upregulated gene 1 (TUG1). In this study, we explored the functional significance and molecular mechanisms of TUG1/miR-132-3p axis in ischemia-challenged cardiomyocytes.

MicroRNA-494 Inhibits the LRG1 Expression to Induce Proliferation and Migration of VECs in Rats following Myocardial Infarction.

Myocardial infarction (MI) is a life-threatening cardiac event that results in extreme damage to the heart muscle. The Wnt signaling pathway has been implicated in the development of heart diseases. Hence, the current study aimed to investigate the role of microRNA (miRNA) in association with the Wnt signaling pathway to identify potential candidates for MI therapy.

Inhibition of lncRNA TUG1 upregulates miR-142-3p to ameliorate myocardial injury during ischemia and reperfusion via targeting HMGB1- and Rac1-induced autophagy.

Background: Long non-coding RNAs (lncRNAs) play a central role in regulating heart diseases. In the present study, we examined the effects of lncRNA taurine up-regulated gene 1 (TUG1) in ischemia/reperfusion (I/R)- or hydrogen peroxide-challenged cardiomyocytes, with specific focus on autophagy-induced cell apoptosis.

Methods: The expressions of miR-142-3p and TUG1 in HO-challenged cardiomyocytes and I/R-injured heart tissue were measured by RT-qPCR.

The mechanism of miR-142-3p in coronary microembolization-induced myocardiac injury via regulating target gene IRAK-1.

Coronary microembolization (CME) is a common complication seen during primary percutaneous coronary intervention (pPCI). CME-induced myocardiac inflammation is the primary cause of myocardiac injury. Dysregulated miR-142-3p has been implicated in multiple cardiovascular diseases and is significantly downregulated in CME-induced myocardial injury.

microRNA-26a-5p affects myocardial injury induced by coronary microembolization by modulating HMGA1.

Coronary microembolization (CME) occurs when atherosclerotic plaque debris is detached during the treatment of acute coronary syndrome with Percutaneous Coronary Intervention (PCI). The complications of distal microvascular embolism, including local myocardial inflammation, are the main causes of myocardial damage and are a strong predictor of poor long-term prognosis and major cardiac adverse events. microRNAs (miRNAs) are involved in the pathophysiological processes of cardiovascular inflammatory diseases.

Role of TLR4/MyD88/NF-κB signaling pathway in coronary microembolization-induced myocardial injury prevented and treated with nicorandil.

Coronary microembolization (CME) is a common complication during the treatment of acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI). Nicorandil can be used to prevent myocardial injury after PCI to reduce the incidence of coronary no-reflow and slow flow, and play a role in myocardial protection, suggesting that its mechanism may be related to the inhibition of CME-induced inflammation of cardiomyocytes. However, the specific mechanism remains unclear.

Pinocembrin protects endothelial cells from oxidized LDL-induced injury.

Oxidized low-density lipoprotein (ox-LDL) is a major risk factor for atherosclerosis and often causes injury to vascular endothelial cells. We found that pinocembrin, a natural antioxidant found in honey and certain herbs, protects human aortic endothelial cells (HAECs) from ox-LDL-induced injury. Pinocembrin suppresses the expression of pro-inflammatory vascular adhesion molecules (VCAM-1, ICAM-1 and E-selectin) and cytokines (TNF-α, IL-1β, and IL-8), as well as ROS production induced by ox-LDL.