ArticleInternational journal of biological sciences2023
N-glycosylation-mediated CD147 accumulation induces cardiac fibrosis in the diabetic heart through ALK5 activation.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- POU2F1 promotes hypertensive cardiac fibrosis by regulating mitochondrial homeostasis through PINK1/Parkin‑dependent mitophagy.Molecular medicine reports · 2026Article
- CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- New therapeutic approaches for fibrosis: harnessing translational regulation.Trends in molecular medicine · 2025Review
- N-acetylglucosaminyltransferase V attenuates myocardial infarction by mediating the insulin-like growth factor 1 receptor signaling pathway.Journal of translational internal medicine · 2025Article
- Exosomes derived from umbilical cord blood NK cells inhibit the progression of pancreatic cancer by targeting ROS-mediated mitochondrial dysfunction.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Article
- Advanced Nanomedicine Delivery Systems for Cardiovascular Diseases: Viral and Non-Viral Strategies in Targeted Therapy.Molecules (Basel, Switzerland) · 2025Review
- Cardiac fibroblast-specific expression of IL-37 confers the protective effects on fibrosis in diabetic cardiomyopathy mice by regulating SOCS3-STAT3 axis.Journal of geriatric cardiology : JGC · 2024Article
- Clinical glycoproteomics: methods and diseases.MedComm · 2024Review
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- Inhibition of N-acetylglucosaminyltransferase V alleviates diabetic cardiomyopathy in mice by attenuating cardiac hypertrophy and fibrosis.Nutrition & metabolism · 2024Article
- Article
- CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma.Respiratory research · 2024Article
- Role of LncRNA MIAT in Diabetic Complications.Current medicinal chemistry · 2024Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has implicated the important role of fibrosis in diabetic cardiomyopathy (DCM), while the underlying mechanism remains unclear. Considering the distinct and overlapping roles of Cluster of Differentiation 147 (CD147) in the pathogenesis of fibrotic diseases, we aim to investigate the role of CD147 in the fibrosis of DCM and explore its underlying mechanism. AAV9-mediated cardiac-specific CD147 silencing attenuated cardiac fibrosis and cardiac function in diabetic mice. CD147 knockdown significantly inhibited high glucose (HG)-induced activation of CFs. Mechanistically, CD147 directly bound to type I transcription growth factor β (TGF-β) receptor I (ALK5), promoting ALK5 activation and endocytosis to induce SMAD2/3 phosphorylation and nuclear translocation. In addition, HG prevented the ubiquitin-proteasome-dependent degradation of CD147 by promoting GNT-V-mediated N-glycosylation. As a result, cardiac-specific CD147 overexpression in control mice mimicked diabetes-induced cardiac fibrosis, aggravating cardiac function. Importantly, CD147 was also upregulated in serum and myocardial specimens from patients with diabetes compared with non-diabetes, accompanied by echocardiographic indices of cardiac dysfunction and excessive collagen deposition. Our study provides the first evidence that CD147 acts as a pivotal factor to promote diabetic cardiac fibrosis, and may contribute to the development of future CD147-based therapeutic strategies for DCM.
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