A bright red fluorescent genetically encoded sensor for lactate imaging.

Lactate plays a crucial role in energy metabolism and greatly impacts protein activities, exerting diverse physiological and pathological effects. Therefore, convenient lactate assays for tracking spatiotemporal dynamics in living cells are desirable. In this paper, we engineered and optimized a red fluorescent protein sensor for l-lactate named FiLa-Red.

Association between non-alcoholic fatty liver disease and risk of incident heart failure: a meta-analysis of observational studies.

Background And Aims: Recent research has associated non-alcoholic fatty liver disease (NAFLD) with an increased risk of atherosclerotic cardiovascular disease. Previous studies that evaluated the association between NAFLD and risk of heart failure (HF) yielded inconsistent results, however. This meta-analysis aimed to evaluate the association between NAFLD and the risk of HF.

α-Linolenic Acid and Risk of Heart Failure: A Meta-Analysis.

The α-linolenic acid is a plant origin n-3 fatty acid that may reduce the risk of cardiovascular disease. However, the effect of α-linolenic acid (ALA) on the risk of heart failure (HF) remains unclear. In this meta-analysis, we aimed to determine the role of ALA in the risk of incident HF.

Non-alcoholic fatty liver disease is associated with increased risk of chronic kidney disease.

Background And Aims: Whether non-alcoholic fatty liver disease (NAFLD) is associated with an increased risk of incident chronic kidney disease (CKD) independent of established cardio-renal risk factors remains controversial. We aimed to provide a quantitative estimate of the association and strength between NAFLD and risk of CKD after adjustment for multiple cardio-renal risk factors.

Methods: We searched electronic databases (PubMed, Embase, and Google Scholar) for studies published from database inception until 30 November 2020.

Prediabetes and the risk of heart failure: A meta-analysis.

Aim: To determine the role of prediabetes in the incidence of heart failure (HF).

Materials And Methods: We searched electronic databases (PubMed, Embase, Google Scholar and OpenGrey) for studies up to 31 December 2020. Studies were included for meta-analysis if they reported adjusted relative risks (RRs) and 95% confidence intervals (CIs) for the risk of HF for prediabetes compared with normoglycaemia.

Electrophysiological manifestations of rare supra-ventricular tachycardias with concealed nodo-ventricular fibers.

Purpose: To clarify the electrophysiological mechanism of supra-ventricular tachycardias (SVT) with concealed nodo-ventricular (NV) fibers.

Methods: We studied the intra-cardiac electrograms during electrophysiological study (EPS) of three cases of SVT which concerned concealed NV fibers. Electrophysiological maneuvers including right ventricular apex entrainments, RS2 stimuli, adenosine triphosphate injection and so on were done for differential diagnosis before ablation.

The YAP/SERCA2a signaling pathway protects cardiomyocytes against reperfusion-induced apoptosis.

Mitochondria and the endoplasmic reticulum (ER) are known to promote cardiac ischemia/reperfusion (I/R) injury. Overexpression of yes-associated protein (YAP) and/or sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) has been shown to protect cardiomyocytes against I/R-induced injury. Here, we show that activation of the YAP/SERCA2a pathway attenuated mitochondrial damage and ER stress (ERS) to maintain cardiomyocyte viability in the setting of I/R injury.

Piwi-interacting RNAs play a role in vitamin C-mediated effects on endothelial aging.

The underlying mechanisms that mediate the effects of vitamin C on endothelial cell aging are widely unknown. To investigate whether Piwi-interacting RNAs (piRNAs) are involved in this process, an endothelial aging model was induced using HO in human umbilical vein endothelial cells (HUVECs) and then treated with vitamin C (VC). Untreated HUVECs without HO exposure were used to serve as the negative control group.

Nonalcoholic fatty liver disease is associated with increased risk of atrial fibrillation.

Background & Aims: Whether nonalcoholic fatty liver disease (NAFLD) is associated with risk of incident atrial fibrillation (AF) independent of established cardiovascular risk factors remains controversial. We aimed to provide a quantitative estimate of the association between NAFLD and risk of AF after adjustment for cardiometabolic risk factors.

Methods: In this study, we searched PubMed and Embase for studies published from database inception until January 31, 2020.

RETRACTED: MicroRNA-208-5p regulates myocardial injury of sepsis mice via targeting SOCS2-mediated NF-κB/HIF-1α pathway.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).

Combination of melatonin and irisin ameliorates lipopolysaccharide-induced cardiac dysfunction through suppressing the Mst1-JNK pathways.

Despite significant advances in therapies in past decades, the mortality rate of septic cardiomyopathy remains high. The aim of this study is to explore the therapeutic effects of combined treatment using melatonin and irisin in a mouse model of lipopolysaccharide (LPS)-mediated septic cardiomyopathy. Our data found that melatonin and irisin could further attenuate LPS-induced myocardial depression.

Therapeutic contribution of melatonin to the treatment of septic cardiomyopathy: A novel mechanism linking Ripk3-modified mitochondrial performance and endoplasmic reticulum function.

The basic pathophysiological mechanisms underlying septic cardiomyopathy have not yet been completely clarified. Disease-specific treatments are lacking, and care is still based on supportive modalities. The aim of our study was to assess the protective effects of melatonin on septic cardiomyopathy, with a focus on the interactions between receptor-interacting protein kinase 3 (Ripk3), the mitochondria, endoplasmic reticulum (ER) and cytoskeletal degradation in cardiomyocytes.

[Effect of hydrogen sulfide on H₂O₂-stimulated primary neonatal rat cardiomyocytes].

Objective: To investigate the effects of hydrogen sulfide (H2S) on H2O2-stimulated primary neonatal rat cardiomyocytes and related mechanism.

Methods: Primary neonatal rat cardiomyocytes were treated with various concentrations of H2O2 (10, 100, 1000 µmol/L) for 24 h to establish the oxidative stress-induced cell injury model after 3 days' conventional culture. In addition, different concentrations of NaHS (1, 10, 100 µmol/L) were added to cardiomyocytes in the absence and presence of 100 µmol/L H2O2 for 24 h.