February 1, 2024Expert Opinion on Therapeutic Targets
TGF-β as a therapeutic target in the infarcted and failing heart: cellular mechanisms, challenges, and opportunities
Key result
Cautious TGF-β inhibition may benefit heart failure patients with overactive fibrosis but requires mechanism-driven classification.
Why the study?
Understanding cell-specific actions of TGF-β is necessary to design therapeutic strategies targeting myocardial fibrosis and remodeling in patients with heart failure.
Design
Review manuscript
Authors
Discussion
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Implication
Requires mechanism-driven selection for TGF-β therapies in HF; extends fibrosis research toward precision trials.
Key Points
- This review aims to explore TGF-β's role in myocardial fibrosis and heart failure, focusing on its cellular mechanisms and therapeutic potential.
- Review and synthesis of existing literature on TGF-β in cardiac conditions.
- Analysis of TGF-β's effects on various cardiac cell types including fibroblasts and cardiomyocytes.
- Discussion of therapeutic implications and challenges in targeting TGF-β.
- TGF-β is activated in infarcted and failing hearts, affecting fibrosis and remodeling.
- While TGF-β promotes scar formation and anti-inflammatory macrophage responses, it may also lead to detrimental remodeling in cardiomyocytes.
- Careful TGF-β inhibition may benefit heart failure patients with excessive fibrogenic responses.
Structured PICO
P
Population
Patients with myocardial disease, including infarcted, remodeling, and failing hearts (HFrEF and HFpEF)
I
Intervention
TGF-β inhibition
This review highlights the complex, cell-specific roles of TGF-β in myocardial fibrosis and heart failure, suggesting that targeted TGF-β inhibition could be a therapeutic strategy for specific patient subsets.
Cite This Study
Nikolaos G. Frangogiannis (2024) conducted a review in Heart failure and myocardial infarction. TGF-β inhibition was evaluated. Cautious TGF-β inhibition may benefit heart failure patients with prolonged or overactive fibrogenic responses, though its pleiotropic effects require mechanism-driven patient classification.