ReviewCells2025
Molecular Mechanisms Underlying Heart Failure and Their Therapeutic Potential.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed.
- Coronary Microvascular Dysfunction: Epidemiology, Pathophysiology, Diagnosis, and Treatment.MedComm · 2026Review
- Heart Failure with Reduced and Mildly Reduced Ejection Fraction: A Network Interpretive Framework of Mechanisms, Phenotypes, and Therapeutic Response.International journal of molecular sciences · 2026Review
- Inhibition of calpain-mediated HMGB1 alleviates cardiac inflammation and dysfunction induced by ultra-processed foods.JCI insight · 2026Article
- Real-world prescription patterns of guideline-recommended therapies in heart failure across China.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Molecular Mechanisms and Multi-Omics Integration in Heart Failure: From Pathophysiology to Precision Medicine.International journal of molecular sciences · 2026Review
- Amino Acid-Derived Metabolic Signature Across Stages of Systolic Dysfunction: Derivation and Internal Evaluation of the HASI (Heart Failure Amino Acid-Derived Systolic Index)-40 Index.International journal of molecular sciences · 2026Article
- Dual Empagliflozin and Sacubitril/Valsartan Therapy Improves Ex Vivo Cardiac Function in a Rat Model of Heart Failure.Biomedicines · 2026Article
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Lipotoxicity in Diabetic Cardiomyopathy: Molecular Basis and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Gene Therapy for Heart Failure: Impact on Mitochondrial Dysfunction.Biomedicines · 2026Review
- Article
- Seeking Novel Personalized and Sex-Specific Strategies for the Prevention and Treatment of Heart Failure Based on the Assessment of β1-Adrenergic Receptor Desensitization: The Contribution to the HEAL ITALIA Project.Current issues in molecular biology · 2026Article
- Advances in Diagnosis and Treatment of Acute and Chronic Heart Failure: A Comprehensive Review.Journal of clinical medicine · 2026Review
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- Sirtuin 1 is a key molecular link between cellular senescence and heart failure.Frontiers in molecular medicine · 2026Review
- Systemic Inflammatory Biomarkers (Interleukin-6, High-Sensitivity C-Reactive Protein, and Neutrophil-to-Lymphocyte Ratio) and Prognosis in Heart Failure: A Meta-Analysis of Prospective Cohort Studies.Journal of clinical medicine · 2025Review
- Effects of Short and Long Exposure to Food Additive Titanium Dioxide (E171) in H9c2 Rat Cardiomyoblasts and in the Hearts of Rats.Cardiovascular toxicology · 2025Article
- Exploring the Potential of Molecular Hydrogen in Different Heart Failure Models: A Review.International journal of molecular sciences · 2025Review
- Integrated analysis of gene networks and cellular functions identifies novel heart failure biomarkers.Hereditas · 2025Article
- Effects of SGLT2 inhibitors on ion channels in heart failure: focus on the endothelium.Basic research in cardiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Heart failure (HF) is a prominent fatal cardiovascular disorder afflicting 3.4% of the adult population despite the advancement of treatment options. Therefore, a better understanding of the pathogenesis of HF is essential for exploring novel therapeutic strategies. Hypertrophy and fibrosis are significant characteristics of pathological cardiac remodeling, contributing to HF. The mechanisms involved in the development of cardiac remodeling and consequent HF are multifactorial, and in this review, the key underlying mechanisms are discussed. These have been divided into the following categories thusly: (i) mitochondrial dysfunction, including defective dynamics, energy production, and oxidative stress; (ii) cardiac lipotoxicity; (iii) maladaptive endoplasmic reticulum (ER) stress; (iv) impaired autophagy; (v) cardiac inflammatory responses; (vi) programmed cell death, including apoptosis, pyroptosis, and ferroptosis; (vii) endothelial dysfunction; and (viii) defective cardiac contractility. Preclinical data suggest that there is merit in targeting the identified pathways; however, their clinical implications and outcomes regarding treating HF need further investigation in the future. Herein, we introduce the molecular mechanisms pivotal in the onset and progression of HF, as well as compounds targeting the related mechanisms and their therapeutic potential in preventing or rescuing HF. This, therefore, offers an avenue for the design and discovery of novel therapies for the treatment of HF.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.