ArticleMolecular medicine reports2021
High glucose‑induced upregulation of CD36 promotes inflammation stress via NF‑κB in H9c2 cells.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
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- Profile of circular RNAs in bovine mammary tissues infected with Staphylococcus aureus.Archives of microbiology · 2025Article
- Review
- Primordial Drivers of Diabetes Heart Disease: Comprehensive Insights into Insulin Resistance.Diabetes & metabolism journal · 2024Review
- Fetal Myocardial Expression of GLUT1: Roles of BPA Exposure and Cord Blood Exosomes in a Rat Model.Cells · 2022Article
- Shenkang Injection for Treating Renal Fibrosis-Metabonomics and Regulation of E3 Ubiquitin Ligase Smurfs on TGF-β/Smads Signal Transduction.Frontiers in pharmacology · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac inflammation serves an important role in the progression of diabetic cardiomyopathy. CD36 (cluster of differentiation 36) mediates inflammation stress in a variety of disease states. The present study investigated CD36 expression in high glucose (HG)‑induced H9c2 cells, whether CD36 upregulation promotes inflammatory stress, and its potential mechanism. HG induced CD36 expression in a time‑dependent manner in cells, which was blocked following CD36 knockout or treatment with N‑acetylcysteine or MitoTEMPO. CD36 translocation to the cell membrane was increased at 72 h by HG stimulation of H9c2 cells. Moreover, CD36 knockout inhibited HG‑induced reactive oxygen species (ROS) generation, tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑1β expression, and nuclear factor (NF)‑κB pathway activation. Further, CD36 knockout reversed metabolic reprogramming, lipid accumulation and AMP‑activated protein kinase activation caused by HG. The aforementioned data suggest that HG‑induced upregulation of CD36 promotes inflammatory stress via NF‑κB in H9c2 cells, mediated by metabolism reprogramming, lipid accumulation and enhanced ROS generation.
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