Development and validation of a nomogram for major adverse cardiovascular events after chronic total occlusion percutaneous coronary intervention for ischemic heart failure.

Background: Chronic total occlusion percutaneous coronary intervention (CTO-PCI) is an available means of revascularization in patients with ischemic heart failure (IHF). However, the prognosis of IHF patients undergoing CTO-PCI remains unclear due to the lack of reliable clinical predictive tools.

Aim: This study aimed to establish a nomogram for major adverse cardiovascular events (MACE) after CTO-PCI in IHF patients.

Myotubularin-Related Protein14 Prevents Neointima Formation and Vascular Smooth Muscle Cell Proliferation by Inhibiting Polo-Like Kinase1.

Background Restenosis is one of the main bottlenecks in restricting the further development of cardiovascular interventional therapy. New signaling molecules involved in the progress have continuously been discovered; however, the specific molecular mechanisms remain unclear. MTMR14 (myotubularin-related protein 14) is a novel phosphoinositide phosphatase that has a variety of biological functions and is involved in diverse biological processes.

E3 ubiquitin ligase RNF5 attenuates pathological cardiac hypertrophy through STING.

Ring-finger protein 5 (RNF5) is an E3 ubiquitin ligase which is expressed in a variety of human tissues. RNF5 is involved in the regulation of endoplasmic reticulum stress, inflammation, and innate immunity and plays an important role in the occurrence and development of various tumors. However, the role of RNF5 in cardiac hypertrophy has not been reported.

Different Doses of Empagliflozin in Patients with Heart Failure with Reduced Ejection Fraction.

It was unclear whether there are discrepancies among the efficacy and safety of different doses of empagliflozin in patients with heart failure with reduced ejection fraction (HFrEF). The aim of this study was to compare the efficacy and safety of 25 mg and 10 mg of empagliflozin in HFrEF patients.In this 3-month, single-center, open-label, randomized, positive-controlled, parallel-group study, 100 patients with HFrEF were divided into two groups, namely, groups A (n = 50) and B (n = 50), which were given 25 mg/day and 10 mg/day of empagliflozin, respectively.

Dapagliflozin and Empagliflozin in Heart Failure with Reduced Ejection Fraction: A Retrospective Study.

Objective: Dapagliflozin 10 mg and empagliflozin 10 mg have been recommended to treat heart failure with reduced ejection fraction (HFrEF), and the purpose of this study was to compare the efficacy and safety of them in HFrEF.

Methods: Two hundred and thirty-three patients with HFrEF admitted to a tertiary hospital of Zhengzhou and commenced to take dapagliflozin 10 mg/d or empagliflozin 10 mg/d were retrospectively included and separated into the dapagliflozin group (=105) and the empagliflozin group (=128). Their cardiac function indices before and after therapy were compared, together with the ratios of adverse events during therapy.

Development and Validation of a Novel Nomogram to Predict Improved Left Ventricular Ejection Fraction in Patients With Heart Failure After Successful Percutaneous Coronary Intervention for Chronic Total Occlusion.

Background: Heart failure with improved left ventricular ejection fraction (HFiEF) is linked to a good clinical outcome. The purpose of this study was to create an easy-to-use model to predict the occurrence of HFiEF in patients with heart failure (HF), 1 year after successful percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) (CTO PCI).

Methods: Patients diagnosed with HF who successfully underwent CTO PCI between January 2016 and August 2019 were included.

OTUB1 alleviates NASH through inhibition of the TRAF6-ASK1 signaling pathways.

Background And Aims: NAFLD is considered as the hepatic manifestation of the metabolic syndrome, which includes insulin resistance, obesity and hyperlipidemia. NASH is a progressive stage of NAFLD with severe hepatic steatosis, hepatocyte death, inflammation, and fibrosis. Currently, no pharmacological interventions specifically tailored for NASH are approved.

Runt-related transcription factor 1 (Runx1) aggravates pathological cardiac hypertrophy by promoting p53 expression.

Cardiac hypertrophy and the resultant heart failure are among the most common causes of morbidity and mortality worldwide; thus, identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Runx1 (Runt-related transcription factor 1) acts as an essential transcription factor that functions in a variety of cellular processes including differentiation, proliferation, tissue growth and DNA damage response. However, relatively little is known about the role of Runx1 in heart, especially cardiac hypertrophy and heart failure.