ReviewCells2023
The Microenvironment of the Pathogenesis of Cardiac Hypertrophy.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 77 citations in OpenAlex.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- Trilobatin Ameliorates Myocardial Hypertrophy by Enhancing Mitophagy Through Activation of the Sentrin-Specific Protease 1/Sirtuin 3 Axis in Spontaneously Hypertensive Rats.Phytotherapy research : PTR · 2026Article
- The value of CMR-derived left atrial strain parameters in differential diagnosis of cardiac amyloidosis and hypertrophic cardiomyopathy.Quantitative imaging in medicine and surgery · 2026Article
- Galectin-3, transforming growth factor beta 1, and brain natriuretic peptide in cardiac remodeling under hyperlipidemic and hyperglycemic stress.Molecular and cellular biochemistry · 2026Article
- Inflammation-Mediated Mechanisms of Arrhythmias After Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2026Review
- CEBPD-MMP8 Axis Contributes to Cardiomyocyte Injury in Septic Shock.Applied biochemistry and biotechnology · 2026Article
- Differential expression of metabolic genes distinguishes physiological from pathological cardiac hypertrophy.BMC cardiovascular disorders · 2026Article
- Rosuvastatin calcium administration and its impact on myocardial microcirculation and postoperative recovery in patients undergoing coronary artery bypass grafting.Journal of cardiothoracic surgery · 2026Article
- Type-1 Ryanodine Receptor Plays an Important Role in Cardiac Hypertrophy and Heart Failure by Increasing Type-2 Ryanodine Receptor-Mediated Calcium Release.International journal of molecular sciences · 2026Article
- TRIM40 Drives Pathological Cardiac Hypertrophy and Heart Failure via Ubiquitination of PKN2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research Progress on the Biological Function, Disease-Driving Mechanism and Clinical Targeting Strategies of G3BP2.Molecules (Basel, Switzerland) · 2026Review
- The Vascular-Immune Cells Crosstalk and Microenvironment in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Review
- Lingguizhugan Decoction Attenuates Angiotensin II-Induced Cardiac Hypertrophy Through the LITAF Signaling Pathway.Combinatorial chemistry & high throughput screening · 2026Article
- Research progress of OTUD7B: from structural function and disease mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Mechanistic study of Shenge powder on myocardial hypertrophy and cardiac lymphatic intervention in TAC-induced mouse models.Frontiers in pharmacology · 2026Article
- Potential Mechanisms of Sodium-Glucose Cotransporter 2 Inhibitors in Regulating Cardiac and Renal Fibrosis.Cardiorenal medicine · 2026Review
- Gastrin ameliorates heart failure and suppresses myocardial remodeling via the JAK2/STAT3 and ERK1/2 pathways.PloS one · 2026Article
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades' advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components.
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What OpenQuestion 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 OpenQuestion graph.