Interventional therapies for chronic heart failure: An overview of recent developments.

Heart failure (HF), the final manifestation of most cardiovascular diseases, has become a major global health concern, affecting millions of individuals. Despite basic drug treatments, patients present with high morbidity and mortality rates. However, recent advancements in interventional therapy have shown promising results in improving the prognosis of patients with HF.

PiRNA CFAPIR inhibits cardiac fibrosis by regulating the muscleblind-like protein MBNL2.

Myocardial fibroblasts transform into myofibroblasts during the progression of cardiac fibrosis, together with excessive cardiac fibroblast proliferation. Hence, the prevention and treatment of cardiac fibrosis are significant factors for inhibiting the development of heart failure. P-element Induced WImpy testis-interacting RNAs (PiRNA) are widely expressed in the heart, but their involvement in cardiac fibrosis has not yet been confirmed.

MBNL2 promotes aging-related cardiac fibrosis via inhibited SUMOylation of Krüppel-like factor4.

Aging-related cardiac fibrosis represents the principal pathological progression in cardiovascular aging. The Muscleblind-like splicing regulator 2 (MBNL2) has been unequivocally established as being associated with cardiovascular diseases. Nevertheless, its role in aging-related cardiac fibrosis remains unexplored.

Calcitonin Inhibits Phenotypic Switching of Aortic Smooth Muscle Cells and Neointimal Hyperplasia through the AMP-Activated Protein Kinase/Mechanistic Target of Rapamycin Pathway.

Calcitonin (CT) is a peptide hormone secreted by the parafollicular C cells of the thyroid gland, salmon calcitonin was originally extracted from the hind cheek of salmon. Neointimal hyperplasia refers to the excessive proliferation and migration of vascular smooth muscle cells (VSMCs). In this study, a rat model of restenosis was employed to explore the impact of calcitonin on neointima proliferation.

Suramin inhibits phenotypic transformation of vascular smooth muscle cells and neointima hyperplasia by suppressing transforming growth factor beta receptor 1 /Smad2/3 pathway activation.

Vascular smooth muscle cells (VSMCs) contribute to neointimal hyperplasia (NIH) after vascular injury, a common feature of vascular remodelling disorders. Suramin is known to exert antitumour effects by inhibiting the proliferation of various tumour cells; however, its effects and mechanism on VSMCs remain unclear. This study investigated the effects of suramin on human aortic smooth muscle cells (HASMCs), rat aortic smooth muscle cells (RASMCs) and NIH to examine its suitability for the prevention of vascular remodelling disorders.

Histological and functional assessment of a Takotsubo cardiomyopathy model established by immobilization stress.

Introduction: Takotsubo cardiomyopathy (TTC), also known as stress-induced cardiomyopathy, resembles acute heart failure syndrome but lacks disease-specific diagnosis and treatment strategies. TTC accounts for approximately 5-6% of all suspected cases of acute coronary syndrome in women. At present, animal models of TTC are often created by large amounts of exogenous catecholamines such as isoproterenol.

Effects of diabetes mellitus and glycemic traits on cardiovascular morpho-functional phenotypes.

Background: The effects of diabetes on the cardiac and aortic structure and function remain unclear. Detecting and intervening these variations early is crucial for the prevention and management of complications. Cardiovascular magnetic resonance imaging-derived traits are established endophenotypes and serve as precise, early-detection, noninvasive clinical risk biomarkers.

HypERlnc attenuates angiotensin II-induced cardiomyocyte hypertrophy via promoting SIRT1 SUMOylation-mediated activation of PGC-1α/PPARα pathway in AC16 cells.

Cardiac hypertrophy is a well-established risk factor for cardiovascular mortality worldwide. According to a recent study, hypoxia-induced endoplasmic reticulum stress regulating long noncoding RNA (HypERlnc) is significantly reduced in the left ventricular myocardium of heart failure (HF) patients compared with healthy controls. However, the effect of HypERlnc on hypertrophy is unclear.

Sonodynamic therapy reduces cardiomyocyte apoptosis through autophagy activated by reactive oxygen species in myocardial infarction.

Myocardial infarction (MI) is lethal to patients because of acute ischemia and hypoxia leading to cardiac tissue apoptosis. Autophagy played a key role in MI through affecting the survival of cardiomyocytes. LncRNA-MHRT (myosin heavy-chain-associated RNA transcripts) was specific to the heart and cardiomyocytes, and inhibition of lncRNA-MHRT transcription under pathological stimuli could cause cardiac hypertrophy and even heart failure (HF).

Integration of proteomic and metabolomic characterization in atrial fibrillation-induced heart failure.

Background: The exact mechanism of atrial fibrillation (AF)-induced heart failure (HF) remains unclear. Proteomics and metabolomics were integrated to in this study, as to describe AF patients' dysregulated proteins and metabolites, comparing patients without HF to patients with HF.

Methods: Plasma samples of 20 AF patients without HF and another 20 with HF were analyzed by multi-omics platforms.

Small ubiquitin-related modifier (SUMO)ylation of SIRT1 mediates (-)-epicatechin inhibited- differentiation of cardiac fibroblasts into myofibroblasts.

Context: (-)-Epicatechin (EPI) is a crucial substance involved in the protective effects of flavanol-rich foods. Previous studies have indicated EPI has a cardioprotective effect, but the molecular mechanisms in inhibition of cardiac fibrosis are unclear.

Objective: We evaluated the effect of EPI in preventing cardiac fibrosis and the underlying molecular mechanism related to the SIRT1-SUMO1/AKT/GSK3β pathway.

Microvesicles, blood cells, and endothelial cells mediate phosphatidylserine-related prothrombotic state in patients with periodontitis.

Background: Phosphatidylserine (PS) is essential for inflammation-associated thrombogenesis, but the exact effect of PS on the prothrombotic state in periodontitis is uncertain. This study aimed to determine the PS-related procoagulant state in patients with periodontitis.

Methods: A total of 138 patients with periodontitis were examined compared with 42 healthy controls.

Neutrophil extracellular traps enhance procoagulant activity and thrombotic tendency in patients with obstructive jaundice.

Background & Aims: Patients with obstructive jaundice (OJ) are considered to be prothrombotic with increased risk of thromboembolism complications. The role of neutrophil extracellular traps (NETs) in procoagulant activity (PCA) and thrombosis risk in patients with OJ is unclear. In this study, we investigated NETs formation in OJ patients and the role of elevated unconjugated bilirubin (UCB) in inducing NETs, resulting in enhanced PCA and endothelial injury.

Trimethylamine N-Oxide is Associated with Heart Failure Risk in Patients with Preserved Ejection Fraction.

Background: Trimethylamine N-oxide (TMAO) has been considered to be an independent risk factor of heart failure (HF).

Objectives: To further determine the plasma levels of TMAO in patients who have HF with preserved ejection fraction (HFpEF), and to analyze the relationship between TMAO and HFpEF risk.

Methods: A total of 57 control participants and 61 patients with HFpEF were recruited.

The correlation between plasma trimethylamine N-oxide level and heart failure classification in northern Chinese patients.

Background: Trimethylamine N-oxide (TMAO) has been identified as a new biomarker of cardiovascular disease. Our aim was to evaluate the plasma levels of TMAO in patients with or without heart failure (HF), and to indicate the correlation between plasma TMAO level and HF classification in northern Chinese patients.

Methods: A total of 112 control participants and 184 HF patients participated in this study.

Phosphatidylserine-exposing blood cells, microparticles and neutrophil extracellular traps increase procoagulant activity in patients with pancreatic cancer.

Patients with pancreatic cancer (PC) are at increased risk of venous thrombosis, but the precise mechanisms of hypercoagulable state in PC remain unclear. We aimed to identify how phosphatidylserine positive (PS) blood cells (BCs), PS microparticles (MPs) and neutrophil extracellular traps (NETs) regulate procoagulant activity (PCA) in PC, and to assess the relationship between PCA and PC staging. A total of 83 PC patients with different stages of disease were compared to 30 healthy controls, with confocal microscopy and flow cytometry used to assess MP and cellular PS exposure.

The correlation between trimethylamine N-oxide, lipoprotein ratios, and conventional lipid parameters in patients with unstable angina pectoris.

Purpose: Trimethylamine N-oxide (TMAO) is recently the main risk factor for coronary heart disease (CHD). Plasma lipid levels are conventionally used to predict coronary risk, but the correlation between TMAO and plasma lipid levels in unstable angina pectoris (UAP) was unclear. Our objective was to compare the plasma level of TMAO to lipoprotein ratios and conventional lipid parameters in UAP patients.

Influence of AS3MT polymorphisms on arsenic metabolism and liver injury in APL patients treated with arsenic trioxide.

Arsenic-induced side effects limit its application in the treatment of acute promyelocytic leukemia (APL). We recently demonstrated that AS3MT 14215 (rs3740390) genotypes were associated with urinary arsenic metabolites and hematological and biochemical values. To further decipher the role of AS3MT genotypes on arsenic metabolism and toxicity, AS3MT 27215 (rs11191446), 35587 (rs11191453), 35991 (rs10748835), and their interactive effects were examined in fifty APL patients treated with arsenic trioxide (AsO) for the first time.

Neutrophil Extracellular Traps Induce Intestinal Damage and Thrombotic Tendency in Inflammatory Bowel Disease.

Background And Aims: Despite the presence of neutrophil extracellular traps [NETs] in inflamed colon having been confirmed, the role of NETs, especially the circulating NETs, in the progression and thrombotic tendency of inflammatory bowel disease [IBD] remains elusive. We extended our previous study to prove that NETs constitute a central component in the progression and prothrombotic state of IBD.

Methods: In all 48 consecutive patients with IBD were studied.

Neutrophil extracellular traps induced by activated platelets contribute to procoagulant activity in patients with colorectal cancer.

Patients with colorectal cancer (CRC) are at increased risk of venous thrombosis, but the precise mechanisms of thrombogenesis in CRC remain largely unknown. We aimed to identify the novel role of neutrophil extracellular traps (NETs) in the induction of procoagulant activity (PCA) in CRC, and to evaluate its interactions with platelets and endothelial cells (ECs). In this study, we first showed that the levels of NETs in the peripheral blood of CRC patients were increased in parallel with cancer progression and reached significance in stage II patients compared to healthy subjects.