ReviewBritish journal of pharmacology2016
Molecular switches under TGFβ signalling during progression from cardiac hypertrophy to heart failure.
Review in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
- Amentoflavone, a Preferentially TGF-β Receptor 1 Inhibitor, Alleviates Cardiac Remodeling and Dysfunction Through Modulating the TGF-β/Smad and MAPK Signaling Pathways.Phytotherapy research : PTR · 2026Article
- Enhancing KLF15 activity in cardiomyocytes: a novel approach to prevent pathological reprogramming and fibrosis via nuclease-deficient dCas9VPR.Signal transduction and targeted therapy · 2026Article
- Bisdemethoxycurcumin attenuates myocardial fibrosis in heart failure with preserved ejection fraction by targeting TGFBR1 and oxidative stress.Computational and structural biotechnology journal · 2026Article
- The Concise Guide to PHARMACOLOGY 2025/26: Catalytic receptors.British journal of pharmacology · 2025Review
- ADAMTS2: More than a procollagen N-proteinase.Genes & diseases · 2025Review
- Uncovering the Therapeutic Potential of Lithium Chloride in Type 2 Diabetic Cardiomyopathy: Targeting Tau Hyperphosphorylation and TGF-β Signaling via GSK-3β Inhibition.Pharmaceutics · 2024Article
- TNIP3 protects against pathological cardiac hypertrophy by stabilizing STAT1.Cell death & disease · 2024Article
- Muscone inhibits angiotensin II-induced cardiac hypertrophy through the STAT3, MAPK and TGF-β/SMAD signaling pathways.Molecular biology reports · 2023Article
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Article
- Status of βReviews in cardiovascular medicine · 2023Review
- Inhibition of the extracellular enzyme A disintegrin and metalloprotease with thrombospondin motif 4 prevents cardiac fibrosis and dysfunction.Cardiovascular research · 2023Article
- Article
- Changes in cellular CaThe Journal of physiology · 2023Article
- SMOC2 plays a role in heart failure via regulating TGF-β1/Smad3 pathway-mediated autophagy.Open medicine (Warsaw, Poland) · 2023Article
- The role of pyroptosis in inflammatory diseases.Frontiers in cell and developmental biology · 2023Review
- Irisin attenuates angiotensin II-induced atrial fibrillation and atrial fibrosis via LOXL2 and TGFβ1/Smad2/3 signaling pathways.Iranian journal of basic medical sciences · 2023Article
- Inhibition of FABP4 attenuates cardiac fibrosis through inhibition of NLRP3 inflammasome activation.Iranian journal of basic medical sciences · 2022Article
- LOXL2 silencing suppresses angiotensin II-induced cardiac hypertrophy through the EMT process and TGF-β1/Smad3/NF-κB pathway.Iranian journal of basic medical sciences · 2022Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is a mechanism to compensate for increased cardiac work load, that is, after myocardial infarction or upon pressure overload. However, in the long run cardiac hypertrophy is a prevailing risk factor for the development of heart failure. During pathological remodelling processes leading to heart failure, decompensated hypertrophy, death of cardiomyocytes by apoptosis or necroptosis and fibrosis as well as a progressive dysfunction of cardiomyocytes are apparent. Interestingly, the induction of hypertrophy, cell death or fibrosis is mediated by similar signalling pathways. Therefore, tiny changes in the signalling cascade are able to switch physiological cardiac remodelling to the development of heart failure. In the present review, we will describe examples of these molecular switches that change compensated hypertrophy to the development of heart failure and will focus on the importance of the signalling cascades of the TGFβ superfamily in this process. In this context, potential therapeutic targets for pharmacological interventions that could attenuate the progression of heart failure will be discussed.
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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.