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Unveiling the role of c-Met: A promising target for cardiovascular disease
Jing Gao1, Xiaocong Wang1, Li Zhang2
1Department of Echocardiography, The First Hospital of Jilin University, Jilin University, Changchun, China.
Insights
Cardiovascular diseases (CVDs) require new treatments. The c-Met signaling pathway shows dual roles in CVDs, offering potential therapeutic targets but needing careful consideration for effective clinical application.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Signal Transduction
Background:
- Cardiovascular diseases (CVDs) are a major global health burden, necessitating novel therapeutic targets.
- The c-Met receptor tyrosine kinase (RTK), activated by hepatocyte growth factor (HGF), is crucial for cellular functions and implicated in various diseases.
Purpose of the Study:
- To review the multifaceted roles of c-Met signaling in cardiovascular health and disease.
- To explore the context-dependent functions of c-Met in conditions like atherosclerosis, myocardial infarction, pulmonary arterial hypertension, myocarditis, and heart failure.
- To discuss current and potential therapeutic strategies targeting c-Met for CVDs.
Main Methods:
- Literature review synthesizing current knowledge on c-Met signaling in cardiovascular contexts.
- Analysis of preclinical data on c-Met's role in various cardiovascular pathologies.
- Examination of emerging therapeutic approaches targeting the c-Met pathway.
Main Results:
- c-Met signaling exhibits paradoxical effects in atherosclerosis, promoting proliferation but also offering anti-apoptotic and anti-fibrotic benefits.
- Preclinical studies indicate cardioprotective effects of c-Met in myocardial infarction, enhancing repair and survival.
- Aberrant c-Met activation can worsen pulmonary arterial hypertension and influence myocarditis and heart failure progression.
Conclusions:
- c-Met signaling presents a complex, context-dependent target for cardiovascular diseases.
- Therapeutic strategies targeting c-Met, including cell therapy and inhibitors, show preclinical promise but require clinical validation.
- Further research into spatiotemporal c-Met mechanisms is essential for developing precision CVD therapies.
Abstract:
Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality, need the exploration of novel biomarkers and therapeutic targets. The c-Met receptor tyrosine kinase（RTK）, activated by hepatocyte growth factor (HGF), plays multifaceted roles in cellular proliferation, survival, angiogenesis, and tissue repair. While extensively studied in oncology, emerging evidence highlights its dual regulatory functions in CVDs pathogenesis. This review synthesizes current knowledge on c-Met signaling in cardiovascular health and disease, emphasizing its context-dependent roles. In atherosclerosis, c-Met exhibits paradoxical effects-promoting vascular smooth muscle cell proliferation and inflammation while exerting anti-apoptotic and anti-fibrotic actions. Preclinical studies reveal its cardioprotective potential in myocardial infarction by enhancing cardiomyocyte survival, angiogenesis, and cardiac repair, yet aberrant c-Met activation may exacerbate pulmonary arterial hypertension via smooth muscle hyperplasia. Furthermore, c-Met influences inflammatory cell dynamics in myocarditis and modulates heart failure progression through interactions with neurohormonal pathways. Therapeutic strategies targeting c-Met, including CAR-M cell therapy, small-molecule inhibitors, and monoclonal antibodies, show promise in preclinical models but require rigorous clinical validation. Key challenges include reconciling its dual roles across disease stages and optimizing therapeutic specificity. Future research must elucidate spatiotemporal c-Met signaling mechanisms to harness its reparative potential while mitigating pathological effects, ultimately advancing precision therapies for CVDs.
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