ReviewPharmacology & therapeutics2012
Regression of pathological cardiac hypertrophy: signaling pathways and therapeutic targets.
Review in Pharmacology & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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
48 citing papers in PubMed, 98 citations in OpenAlex.
- Regular consumption of green tea improves pulse pressure and induces regression of left ventricular hypertrophy in hypertensive patients.Physiological reports · 2019Trial
- TRIM40 Drives Pathological Cardiac Hypertrophy and Heart Failure via Ubiquitination of PKN2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Galangin 3-methyl ether alleviates mouse hypertrophic cardiomyopathy via targeting HDAC2 and subsequently inactivating the PI3K-AKT signaling pathway.Acta pharmacologica Sinica · 2026Article
- Endothelial LRRC8A mitigates pressure overload-induced cardiac hypertrophy by promoting coronary angiogenesis.Angiogenesis · 2025Article
- Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.European journal of pharmacology · 2025Review
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- Regulatory mechanisms of exercise-induced physiological cardiac hypertrophy: progress and prospects.Frontiers in cardiovascular medicine · 2025Review
- Jaranol: a compound with therapeutic activity against pathological cardiac remodelling via multi-target inhibition of the Snai3/TLR2 and NF-κB signaling pathways.Frontiers in pharmacology · 2025Article
- Mast Cells Contribute to Pressure Overload-Induced Myocardial Hypertrophy by Upregulating TRPV4 via Histamine: Role of Ca2+/ CnA/NFATc3 Signaling Pathway.Current medical science · 2024Article
- LncRNA CCAT2 Knockdown Alleviates Pressure Overload or Ang II-Induced Cardiac Hypertrophy Via Disruption of the Wnt/β-Catenin Signaling.Arquivos brasileiros de cardiologia · 2024Article
- CircSMAD3 represses SMAD3 phosphorylation and ameliorates cardiac remodeling by recruiting YBX1.iScience · 2024Article
- Muscone inhibits angiotensin II-induced cardiac hypertrophy through the STAT3, MAPK and TGF-β/SMAD signaling pathways.Molecular biology reports · 2023Article
- Made in the Womb: Maternal Programming of Offspring Cardiovascular Function by an Obesogenic Womb.Metabolites · 2023Review
- The role of pyroptosis in inflammatory diseases.Frontiers in cell and developmental biology · 2023Review
- Extracellular Vesicles and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023Article
- Involvement of circRNAs in the Development of Heart Failure.International journal of molecular sciences · 2022Review
- Activating transcription factor 3 inhibits angiotensin II‑induced cardiomyocyte viability and fibrosis by activating the transcription of cysteine‑rich angiogenic protein 61.Molecular medicine reports · 2022Article
- Shunxin decoction improves diastolic function in rats with heart failure with preserved ejection fraction induced by abdominal aorta constriction through cyclic guanosine monophosphate-dependent protein kinase Signaling Pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- CHIR99021 Promotes hiPSC-Derived Cardiomyocyte Proliferation in Engineered 3D Microtissues.Advanced healthcare materials · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Pathological cardiac hypertrophy is a key risk factor for heart failure. It is associated with increased interstitial fibrosis, cell death and cardiac dysfunction. The progression of pathological cardiac hypertrophy has long been considered as irreversible. However, recent clinical observations and experimental studies have produced evidence showing the reversal of pathological cardiac hypertrophy. Left ventricle assist devices used in heart failure patients for bridging to transplantation not only improve peripheral circulation but also often cause reverse remodeling of the geometry and recovery of the function of the heart. Dietary supplementation with physiologically relevant levels of copper can reverse pathological cardiac hypertrophy in mice. Angiogenesis is essential and vascular endothelial growth factor (VEGF) is a constitutive factor for the regression. The action of VEGF is mediated by VEGF receptor-1, whose activation is linked to cyclic GMP-dependent protein kinase-1 (PKG-1) signaling pathways, and inhibition of cyclic GMP degradation leads to regression of pathological cardiac hypertrophy. Most of these pathways are regulated by hypoxia-inducible factor. Potential therapeutic targets for promoting the regression include: promotion of angiogenesis, selective enhancement of VEGF receptor-1 signaling pathways, stimulation of PKG-1 pathways, and sustention of hypoxia-inducible factor transcriptional activity. More exciting insights into the regression of pathological cardiac hypertrophy are emerging. The time of translating the concept of regression of pathological cardiac hypertrophy to clinical practice is coming.
Indexed as
Identifiers
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.