ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2020
CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Diagnostic and Prognostic Potential of Tetranectin in Heart Failure and Cardiovascular Disease: A Systematic Review.Medical sciences (Basel, Switzerland) · 2025Pooled it
- Tetranectin as a Potential Biomarker Associated with Post-Operative Inotropic Support Following the Norwood Procedure in Neonates: A Pilot Study.Journal of cardiovascular development and disease · 2026Article
- Epigenetic signatures of cardiometabolic risk in men: accelerated aging and differential methylation replicated across cohorts.Clinical epigenetics · 2026Article
- Unveiling the Mysteries of CLEC3B: Physiological Roles, Pathological Impacts, and Research Gaps.Cells · 2026Review
- RIPK4 function interferes with melanoma cell adhesion and metastasis.Molecular oncology · 2026Article
- Article
- The Anti-Myogenic Role of Tetranectin and Its Inhibition by Epigallocatechin-3-Gallate Enhances Myogenesis.Cells · 2025Article
- Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not well-characterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (P<0.05). Overexpression of CLEC3B increased cell viability (P<0.01), inhibited cell apoptosis (P<0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (P<0.01 or P<0.05), and downregulated expression of cleaved-caspase 3 (P<0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.
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