ArticleExperimental and therapeutic medicine2017
Transforming growth factor β and its role in heart disease.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 97 citations in OpenAlex.
- BMAL1 attenuates myocardial infarction-induced fibrosis via suppressing p-SMAD3/SMAD3 in TGF-β1 pathway.Biochemistry and biophysics reports · 2026Article
- Identification of Hypoxia-Related Genes in Human Myocardial Infarction and Cancers.Cardiology · 2026Article
- The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Article
- Vitamin B17 alleviates Sorafenib-induced cardiotoxicity in Ehrlich Ascites Carcinoma mice via modulation of inflammatory and fibrotic pathways.Scientific reports · 2025Article
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- Association Between Redox and Inflammatory Biomarkers with the Presence and Severity of Obstructive Sleep Apnea.Medicina (Kaunas, Lithuania) · 2025Article
- 17(R)-Resolvin D1 protects against sickle cell-related inflammatory cardiomyopathy in humanized mice.Blood · 2025Article
- Prognostic value of platelet volume indices in heart failure: a systematic review and meta-analysis.American journal of blood research · 2025Review
- Effect of sodium-glucose Co-transporter 2 inhibitors on coronary microcirculation.Frontiers in pharmacology · 2025Review
- Integrative Bioinformatics Approaches to Uncover Hub Genes and Pathways Involved in Cardiovascular Diseases.Cell biochemistry and biophysics · 2024Article
- Inflammation, Oxidative Stress, and Endothelial Dysfunction in the Pathogenesis of Vascular Damage: Unraveling Novel Cardiovascular Risk Factors in Fabry Disease.International journal of molecular sciences · 2024Review
- 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
- A common gene signature of the right ventricle in failing rat and human hearts.Nature cardiovascular research · 2024Article
- Neuronal nitric oxide synthase required for erythropoietin modulation of heart function in mice.Frontiers in physiology · 2024Article
- Compromised diabetic heart function is not affected by miR-378a upregulation upon hyperglycemia.Pharmacological reports : PR · 2023Article
- Effects of Doxorubicin on Extracellular Matrix Regulation in Primary Cardiac Fibroblasts from Mice.BMC research notes · 2023Article
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Article
- Endothelial-derived extracellular vesicles from obese/hypertensive adults increase factors associated with hypertrophy and fibrosis in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2023Article
- Coronary Artery Spasm-Related Heart Failure Syndrome: Literature Review.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is a major form of heart disease that leads to immediate cardiomyocyte death due to ischemia and eventually fibrosis and scar formation and further dysfunction of myocardium and heart failure. Extracellular matrix (ECM) production and tissue repair is conducted by myofibroblasts, which are formed from the normal quiescent cardiac fibroblasts following transformational changes, through the active participation of transforming growth factor β (TGFβ) and its signaling pathways. TGFβ appears to be a 'Master of all trades', with respect to cardiac fibrosis, as it can promote cardiomyocyte apoptosis and cardiac hypertrophy. TGFβ signaling involves its binding to TGFβ receptor type II (TGFβRII), which recruits TGFβ receptor type I (TGFβRI), which are also known as activin receptor-like kinase (ALK) in five different isoforms. In canonical signaling pathways, ALK5 activates Smads 2 and 3, and ALK1 activates Smads 1 and 5. These pairs of Smads form a corresponding complex and then bind to Smad 4, to translocate into the nucleus, where transcriptional reprogramming is carried out to promote myofibroblast formation and ECM production, eventually leading to cardiac fibrosis. TGFβ levels are elevated in MI, thereby aggravating the myocardial injury further. Several microRNAs are involved in the regulation of TGFβ signaling at different steps, affecting different components. Therapeutic targeting of TGFβ signaling at ALK1-5 receptor activity level has met with limited success and extensive research is needed to develop therapies based on the components of TGFβ signaling pathway, for instance cardiac dysfunction and heart failure.
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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.