Dapagliflozin inhibits ferroptosis and ameliorates renal fibrosis in diabetic C57BL/6J mice.

Diabetic nephropathy (DN) is a common complication of diabetes and a major cause of end-stage renal disease, with complex pathogenesis involving inflammation, oxidative stress, fibrosis, and ferroptosis. Ferroptosis is linked to DN progression, yet treatment options are limited, particularly for targeting ferroptosis. Dapagliflozin (DAPA), an SGLT2 inhibitor, shows renal protective effects in diabetes, but its role in renal fibrosis and ferroptosis in DN is unclear.

S100A12 triggers NETosis to aggravate myocardial infarction injury via the Annexin A5-calcium axis.

Neutrophil extracellular traps (NETs) play a critical role in acute myocardial infarction (AMI) and the externalization of S100 family members. Here, we show the effects of S100A12 on NETs formation and myocardial injury following AMI. S100A12 expression increases rapidly in neutrophils and peaks on day 1 after AMI, promoting NETs production and exacerbating myocardial injury.

Identification of critical endoplasmic reticulum stress-related genes in advanced atherosclerotic plaque.

Atherosclerosis (AS) is the principal pathological cause of atherosclerotic cardiovascular diseases. Chronic endoplasmic reticulum stress (ERS) has been implicated in AS aetiopathogenesis, but the underlying molecular interactions remain unclear. This study aims to identify the molecular mechanisms of ERS in AS pathogenesis to inform innovative diagnostic approaches and therapeutic targets for managing AS.

TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway.

Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro.

Integrating network pharmacology and experimental verification to explore the pharmacological mechanisms of Guanxin Shutong capsule in treating heart failure.

The Guanxin Shutong capsule (GXST), a traditional Chinese medicine, is commonly used for treating cardiovascular disease, it has shown efficacy in improving symptoms and enhancing the quality of life for patients with heart failure (HF). However, the specific mechanism of action of GXST in HF remains unclear. In this study, we employed a comprehensive approach combining network pharmacology, molecular dynamics (MD) simulations, and in vitro validations to investigate the potential targets and molecular mechanisms of GXST against HF.

The role of mitofusin 2 in regulating endothelial cell senescence: Implications for vascular aging.

Endothelial cell dysfunction contributes to age-related vascular diseases. Analyzing public databases and mouse tissues, we found decreased MFN2 expression in senescent endothelial cells and angiotensin II-treated mouse aortas. In human endothelial cells, Ang II reduced MFN2 expression while increasing senescence markers P21 and P53.

Identification of hub modules and therapeutic targets associated with CD8T-cells in HF and their pan-cancer analysis.

Heart failure (HF) is a terminal condition of multiple cardiovascular disorders. Cancer is a deadly disease worldwide. The relationship between HF and cancer remains poorly understood.

CREG1 attenuates doxorubicin-induced cardiotoxicity by inhibiting the ferroptosis of cardiomyocytes.

Objective: Doxorubicin (DOX)-induced cardiotoxicity limits the application of DOX in cancer patients. Currently, there is no effective prevention or treatment for DOX-induced cardiotoxicity. The cellular repressor of E1A-stimulated genes (CREG1) is a cardioprotective factor that plays an important role in the maintenance of cardiomyocytes differentiation and homeostasis.

Unraveling shared molecular signatures and potential therapeutic targets linking psoriasis and acute myocardial infarction.

Psoriasis, a chronic inflammatory skin disorder, is associated with comorbidities such as acute myocardial infarction (AMI). However, the molecular mechanisms connecting these conditions are unclear. In this study, we conducted bioinformatics analyses using gene expression datasets to identify differentially expressed genes and hub genes associated with both psoriasis and AMI.

Unveiling shared biomarkers and therapeutic targets between systemic lupus erythematosus and heart failure through bioinformatics analysis.

Background: Systemic lupus erythematosus (SLE) is frequently accompanied by various complications, with cardiovascular diseases being particularly concerning due to their high mortality rate. Although there is clinical evidence suggesting a potential correlation between SLE and heart failure (HF), the underlying shared mechanism is not fully understood. Therefore, it is imperative to explore the potential mechanisms and shared therapeutic targets between SLE and HF.

Single-cell transcriptomics in MI identify Slc25a4 as a new modulator of mitochondrial malfunction and apoptosis-associated cardiomyocyte subcluster.

Myocardial infarction (MI) is the leading cause of premature death. The death of cardiomyocytes (CMs) and the dysfunction of the remaining viable CMs are the main pathological factors contributing to heart failure (HF) following MI. This study aims to determine the transcriptional profile of CMs and investigate the heterogeneity among CMs under hypoxic conditions.

CREG1 deficiency impaired myoblast differentiation and skeletal muscle regeneration.

Background: CREG1 (cellular repressor of E1A-stimulated genes 1) is a protein involved in cellular differentiation and homeostasis regulation. However, its role in skeletal muscle satellite cells differentiation and muscle regeneration is poorly understood. This study aimed to investigate the role of CREG1 in myogenesis and muscle regeneration.

Unraveling the molecular links between benzopyrene exposure, NASH, and HCC: an integrated bioinformatics and experimental study.

Benzopyrene (B[a]P) is a well-known carcinogen that can induce chronic inflammation and fibrosis in the liver, leading to liver disease upon chronic exposure. Nonalcoholic steatohepatitis (NASH) is a chronic liver condition characterized by fat accumulation, inflammation, and fibrosis, often resulting in hepatocellular carcinoma (HCC). In this study, we aimed to investigate the intricate connections between B[a]P exposure, NASH, and HCC.

The CREG1-FBXO27-LAMP2 axis alleviates diabetic cardiomyopathy by promoting autophagy in cardiomyocytes.

Autophagy plays an important role in the development of diabetic cardiomyopathy. Cellular repressor of E1A-stimulated genes 1 (CREG1) is an important myocardial protective factor. The aim of this study was to investigate the effects and mechanisms of CREG1 in diabetic cardiomyopathy.

The role of CREG1 in megakaryocyte maturation and thrombocytopoiesis.

Abnormal megakaryocyte maturation and platelet production lead to platelet-related diseases and impact the dynamic balance between hemostasis and bleeding. Cellular repressor of E1A-stimulated gene 1 (CREG1) is a glycoprotein that promotes tissue differentiation. However, its role in megakaryocytes remains unclear.

FGF21-FGFR1 controls mitochondrial homeostasis in cardiomyocytes by modulating the degradation of OPA1.

Fibroblast growth factor 21 (FGF21) is a pleiotropic hormone secreted primarily by the liver and is considered a major regulator of energy homeostasis. Recent research has revealed that FGF21 could play an important role in cardiac pathological remodeling effects and prevention of cardiomyopathy; however, the underlying mechanism remains largely unknown. This study aimed to determine the mechanism underlying the cardioprotective effects of FGF21.

MicroRNA-574-5p targeting HOXC6 expression inhibits the hepatocyte lipid uptake to alleviate non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is one of the main causes of liver disease that has reached its last stage. Over the past few years, evidence for miRNAs' centrality in NAFLD pathogenesis has accumulated. According to some studies, miR-574-5p plays a role in lipid metabolism.

Corrigendum to "Orosomucoid 1 Attenuates Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes via Nrf2 Signaling".

[This corrects the article DOI: 10.1155/2020/5923572.].

Gut microbiota induces high platelet response in patients with ST segment elevation myocardial infarction after ticagrelor treatment.

Background: Ticagrelor is a first-line drug for the treatment of acute ST elevation myocardial infarction (STEMI). However, approximately 20% STEMI patients taking ticagrelor exhibited a delayed response and the mechanism was still unclear.

Methods: To explore the mechanism of the poor response of ticagrelor in post-percutaneous coronary intervention (PCI) patients, we enrolled 65 high platelet reactivity (HPR) patients and 90 controls (normal platelet reactivity [NPR]).

Overexpression of MFN2 alleviates sorafenib-induced cardiomyocyte necroptosis via the MAM-CaMKIIδ pathway and .

The continued success of oncological therapeutics is dependent on the mitigation of treatment-related adverse events, particularly cardiovascular toxicities. As such, there is an important need to understand the basic mechanisms of drug toxicities in the process of antitumor therapy. Our aim in this study was to elucidate the underlying mechanisms of sorafenib (sor)-induced cardiomyocyte damage.

HOXA5-miR-574-5p axis promotes adipogenesis and alleviates insulin resistance.

Differentiation of preadipocytes into functional adipocytes could be a major target for repressing obesity-induced insulin resistance (IR). However, the molecular mechanisms involved in adipogenesis and the development of IR are unclear. We report, for the first time, that miR-574-5p, a novel miRNA, promotes adipogenesis to suppress IR.

CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.

Phenotype switching of cardiac fibroblasts into myofibroblasts plays important role in cardiac fibrosis following myocardial infarction (MI). Cellular repressor of E1A-stimulated genes (CREG) protects against vascular and cardiac remodeling induced by angiotensin-II. However, the effects and mechanisms of CREG on phenotype switching of cardiac fibroblasts after MI are unknown.

Thrombopoietic effects of CCAAT/enhancer-binding protein β on the early-stage differentiation of megakaryocytes.

CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor that is involved in adipocytic and monocytic differentiation. However, the physiological role of C/EBPβ in megakaryocytes (MKs) is not clear. In this study, we investigated the effects of C/EBPβ on the early-stage differentiation of MKs, and explored the potential mechanisms of action.

CREG1 improves the capacity of the skeletal muscle response to exercise endurance via modulation of mitophagy.

CREG1 (cellular repressor of E1A-stimulated genes 1) is involved in tissue homeostasis and influences macroautophagy/autophagy to protect cardiovascular function. However, the physiological and pathological role of CREG1 in the skeletal muscle is not clear. Here, we established a skeletal muscle-specific knockout mouse model () by crossing the -floxed mice () with a transgenic line expressing recombinase under the muscle-specific (creatine kinase, muscle) promoter.

Overexpression of Kininogen-1 aggravates oxidative stress and mitochondrial dysfunction in DOX-induced cardiotoxicity.

Background: Doxorubicin (DOX) is a widely used cancer chemotherapeutic drug with cardiotoxicity effect limiting its clinical use. DOX induced cardiotoxicity is mediated by oxidative stress and mitochondrial damage. Kininogen-1(KNG1) is an important pro-inflammatory and pro-oxidant factor, and studies have found that it can aggravate lung and brain damage.