The role of Smad signaling cascades in cardiac fibrosis
Open accessAbstract
Most myocardial pathologic conditions are associated with cardiac fibrosis, the expansion of the cardiac interstitium through deposition of extracellular matrix (ECM) proteins. Although replacement fibrosis plays a reparative role after myocardial infarction, excessive, unrestrained or dysregulated myocardial ECM deposition is associated with ventricular dysfunction, dysrhythmias and adverse prognosis in patients with heart failure. The members of the Transforming Growth Factor (TGF)-β superfamily are critical regulators of cardiac repair, remodeling and fibrosis. TGF-βs are released and activated in injured tissues, bind to their receptors and transduce signals in part through activation of cascades involving a family of intracellular effectors the receptor-activated Smads (R-Smads). This review manuscript summarizes our knowledge on the role of Smad signaling cascades in cardiac fibrosis. Smad3, the best-characterized member of the family plays a critical role in activation of a myofibroblast phenotype, stimulation of ECM synthesis, integrin expression and secretion of proteases and anti-proteases. In vivo, fibroblast Smad3 signaling is critically involved in scar organization and exerts matrix-preserving actions. Although Smad2 also regulates fibroblast function in vitro, its in vivo role in rodent models of cardiac fibrosis seems more limited. Very limited information is available on the potential involvement of the Smad1/5/8 cascade in cardiac fibrosis. Dissection of the cellular actions of Smads in cardiac fibrosis, and identification of patient subsets with overactive or dysregulated myocardial Smad-dependent fibrogenic responses are critical for design of successful therapeutic strategies in patients with fibrosis-associated heart failure.
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Motif analysis of these regions revealed enrichment for profibrotic TFs such as SMADs and MEOX1, and for RUNX1 and REL, regulators of proinflammatory responses.
“Motif analysis of these regions revealed enrichment for TFs critical for profibrotic responses in heart failure, such as SMADs27 and MEOX14, as well as RUNX1 and REL, regulators of proinflammatory responses27 (Extended Data Fig. 4D).”
From Chromatin remodelling drives immune cell–fibroblast communication in heart failure (2024) · cites this paper as [27]
The ‘Smad signaling cascades in fibroblasts’ section (page not provided) describes Smad3 as a central signal promoting cardiac myofibroblast conversion and extracellular-matrix production, supporting the profibrotic role attributed to SMADs. The passages retrieved for RUNX1 and REL do not establish their roles in proinflammatory responses. The motif enrichment is presented as the citing paper’s own analysis, and MEOX1 carries a different citation. (LLM, conf=0.86)
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Cited by
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Chromatin remodelling drives immune cell–fibroblast communication in heart failure
Alexanian, M., Padmanabhan, A., Nishino, T., Travers, J. G., Ye, L., Pelonero, A., Lee, C. Y., Sadagopan, N., Huang, Y., Auclair, K., et al. (2024) · Nature · doi:10.1038/s41586-024-08085-6 · Cited by 140 · see citing works
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- Authors
- Hanna, A., Humeres, C., & Frangogiannis, N. G.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Frangogiannis, Nikolaos G.
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 77
- Pages
- 109826
- ISSN
- 0898-6568 (ISSN-L)
- PMC
- PMC7727442
- OpenAlex
- W3096166596
- Cited by
- 132
- References
- 167
- Citations by year
- 2026: 23 · 2025: 18 · 2024: 30 · 2023: 21 · 2022: 26 · 2021: 14
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 308 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cellular Signalling (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (19POST34450144)
- National Heart, Lung, and Blood Institute (HL85440, HL76246, R01 HL149407)
- National Institutes of Health
- U.S. Department of Defense (PR151029, PR181464, PR151134)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- myocardial fibrosis, Smad signaling, Smad3, Smad2, Smad1/5/8, TGF-beta superfamily, extracellular matrix deposition, myofibroblast phenotype, fibroblast activation, heart failure, cardiac remodeling, integrin expression, protease secretion, cardiac repair
- MeSH terms
- Animals, Diabetes Mellitus, Humans, Myocardial Infarction, Signal Transduction, Extracellular Matrix Proteins, Smad Proteins, TGF-beta Superfamily Proteins, Myofibroblasts
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