molecular-mechanisms-dbnl-heart-failure-from-macrophage

Molecular Mechanisms of DBNL in Heart Failure: From Macrophage Immunometabolism to Therapeutic Implications

Heart failure (HF) remains a major global health challenge, with limited effective treatments targeting its core pathophysiological mechanisms. In this ...

The First Affiliated Hospital of Ningbo University

A number of researches have evaluated the association between the ABCB1 polymorphism and the lipid-lowering response of statins, but the results have been inconclusive. To examine the lipid-lowering efficacy and safety associated with the ABCB1 C3435T polymorphism in hypercholesterolemic patients receiving statin, all available studies were included in this meta-analysis.

ABCB1 C3435T polymorphism and the lipid-lowering response in hypercholesterolemic patients on statins: a meta-analysis.

Clopidogrel resistance profoundly increases the risk of major cardiovascular events in coronary artery disease (CAD) patients. Here, we comprehensively analyse global m6A modification alterations in clopidogrel-resistant (CR) and non-CR patients.

Transcriptome-wide map of N6-methyladenosine (m6A) profiling in coronary artery disease (CAD) with clopidogrel resistance.

Clopidogrel resistance (CR) increases the risk of atherothrombotic events. Emerging evidence suggests that circRNAs may influence pharmacodynamic responses to clopidogrel.

Identification of hsa_circ_0076957 and miR-4512-targeted COL19A1 as regulators in clopidogrel resistance among stable coronary heart disease patients through comprehensive circRNA and miRNA analysis.

The use of doxorubicin (DOX), a potent chemotherapy drug, is limited by its detrimental effects on the heart. This cardiotoxicity is primarily driven by oxidative stress and inflammation. TRIM35 plays a key role in inflammatory responses; however, its exact function in DOX-induced cardiotoxicity (DIC) remains to be fully understood. This study investigates the effects of TRIM35 on DIC and explores the underlying biological mechanisms.

Downregulated TRIM35 Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Inflammation via Inhibiting TLR4/NF-κB Pathway.

Doxorubicin-induced cardiomyopathy (DCM) remains a major clinical challenge, highlighting the need for early diagnostic biomarkers. Exosomal miRNAs are promising candidates due to their stability and regulatory functions in cardiovascular diseases.

Article	Year
ABCB1 C3435T polymorphism and the lipid-lowering response in hypercholesterolemic patients on statins: a meta-analysis. Lipids in health and disease\| PubMed ID: 26438079	2015
Transcriptome-wide map of N6-methyladenosine (m6A) profiling in coronary artery disease (CAD) with clopidogrel resistance. Clinical epigenetics\| PubMed ID: 38098098	2023
Identification of hsa_circ_0076957 and miR-4512-targeted COL19A1 as regulators in clopidogrel resistance among stable coronary heart disease patients through comprehensive circRNA and miRNA ... European journal of pharmacology\| PubMed ID: 39615866	2025
Downregulated TRIM35 Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Inflammation via Inhibiting TLR4/NF-κB Pathway. Cardiovascular drugs and therapy\| PubMed ID: 39954170	2025
Role of myocardium-derived exosomal miRNAs in doxorubicin-induced cardiomyopathy. Gene\| PubMed ID: 41115580	2026

Jia Su

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