ArticleBioMed research international2017
Downregulation of Profilin-1 Expression Attenuates Cardiomyocytes Hypertrophy and Apoptosis Induced by Advanced Glycation End Products in H9c2 Cells.
Article in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- The Role of Advanced Glycation End-Products in the Pathophysiology and Pharmacotherapy of Cardiovascular Disease.International journal of molecular sciences · 2025Review
- Transcriptome analysis of the cerebral cortex of acrylamide-exposed wild-type and IL-1β-knockout mice.Archives of toxicology · 2024Article
- Article
- Article
- Profilin1 Promotes Renal Tubular Epithelial Cell Apoptosis in Diabetic Nephropathy Through the Hedgehog Signaling Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Actin-Binding Proteins in Cardiac Hypertrophy.Cells · 2022Review
- Effect of profilin-1 on the asymmetric dimethylarginine-induced vascular lesion-associated hypertension.The Kaohsiung journal of medical sciences · 2022Article
- Selenium Supplementation Improved Cardiac Functions by Suppressing DNMT2-MediatedOxidative medicine and cellular longevity · 2022Article
- Profilin-1 is involved in macroangiopathy induced by advanced glycation end productsWorld journal of diabetes · 2021Article
- Review
- The role of profilin-1 in cardiovascular diseases.Journal of cell science · 2021Review
- Profilin-1; a novel regulator of DNA damage response and repair machinery in keratinocytes.Molecular biology reports · 2021Article
- Harnessing the Power of Eph/ephrin Biosemiotics for Theranostic Applications.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Profilin choreographs actin and microtubules in cells and cancer.International review of cell and molecular biology · 2020Article
- Novel ASK1 inhibitor AGI-1067 improves AGE-induced cardiac dysfunction by inhibiting MKKs/p38 MAPK and NF-κB apoptotic signaling.FEBS open bio · 2018Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocytes hypertrophy and apoptosis induced by advanced glycation end products (AGEs) is the crucial pathological foundation contributing to the onset and development of diabetic cardiomyopathy (DCM). However, the mechanism remains poorly understood. Here, we report that profilin-1 (PFN-1), a well-known actin-binding protein, serves as a potent regulator in AGEs-induced cardiomyocytes hypertrophy and apoptosis. PFN-1 was upregulated in AGEs-treated H9c2 cells, which was associated with increased cardiomyocytes hypertrophy and apoptosis. Silencing PFN-1 expression remarkably attenuated AGEs-induced H9c2 cell hypertrophy and apoptosis. Mechanistically, AGEs increased PFN-1 expression through elevating ROS production and RhoA and ROCK2 expression. Consequently, elevated PFN-1 promoted actin cytoskeleton disorganization. When either ROS production/ROCK activation was blocked or cells were treated with Cytochalasin D (actin depolymerizer), H9c2 cells were protected against AGEs-induced cardiac myocyte abnormalities, concomitantly with downregulated expression of PFN-1 and improved actin cytoskeleton alteration. Collectively, these data suggest that PFN-1 may play an important role in AGEs-induced hypertrophy and apoptosis in H9c2 cells.
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