ArticleBioMed research international2016
HSP27 Inhibits Homocysteine-Induced Endothelial Apoptosis by Modulation of ROS Production and Mitochondrial Caspase-Dependent Apoptotic Pathway.
Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 54 citations in OpenAlex.
- Ac-SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes.Animal models and experimental medicine · 2026Article
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- Relationship between plasma homocysteine and clinical grading of varicocele.Asian journal of andrology · 2025Article
- The Protective Role of Heat Shock Proteins against Stresses in Animal Breeding.International journal of molecular sciences · 2024Review
- Article
- Ascorbic acid mitigates the impact of oxidative stress in a human model of febrile seizure and mesial temporal lobe epilepsy.Scientific reports · 2024Article
- Article
- The role of heat shock proteins in the pathogenesis of heart failure (Review).International journal of molecular medicine · 2023Review
- Review
- HSPB1 Regulates Autophagy and Apoptosis in Vascular Smooth Muscle Cells in Arteriosclerosis Obliterans.Cardiovascular therapeutics · 2022Article
- Icaritin alleviates docetaxel-induced skin injury by suppressing reactive oxygen species via estrogen receptors.Thoracic cancer · 2022Article
- Heat Shock Protein 27 Levels Predict Myocardial Inhomogeneities in Hemodialysis Patients.Mediators of inflammation · 2022Article
- Personalized medicine of non-gene-specific chemotherapies for non-small cell lung cancer.Acta pharmaceutica Sinica. B · 2021Review
- Article
- Homocysteine in Neurology: A Possible Contributing Factor to Small Vessel Disease.International journal of molecular sciences · 2021Review
- Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems.International journal of molecular sciences · 2020Review
- Melatonin and vitamin E alleviate homocysteine-induced oxidative injury and apoptosis in endothelial cells.Molecular biology reports · 2020Article
- The Yin and Yang of Alarmins in Regulation of Acute Kidney Injury.Frontiers in medicine · 2020Review
- Intermittent Hypoxic Exposure Reduces Endothelial Dysfunction.BioMed research international · 2020Article
- Anti-Oxidant and Anti-Endothelial Dysfunctional Properties of Nano-Selenium in vitro and in vivo of Hyperhomocysteinemic Rats.International journal of nanomedicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives. Elevated plasma homocysteine (Hcy) could lead to endothelial dysfunction and is viewed as an independent risk factor for atherosclerosis. Heat shock protein 27 (HSP27), a small heat shock protein, is reported to exert protective effect against atherosclerosis. This study aims to investigate the protective effect of HSP27 against Hcy-induced endothelial cell apoptosis in human umbilical vein endothelial cells (HUVECs) and to determine the underlying mechanisms. Methods. Apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) of normal or HSP27-overexpressing HUVECs in the presence of Hcy were analyzed by flow cytometry. The mRNA and protein expression levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Results. We found that Hcy could induce cell apoptosis with corresponding decrease of nitric oxide (NO) level, increase of endothelin-1 (ET-1), intracellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) levels, elevation of ROS, and dissipation of MMP. In addition, HSP27 could protect the cell against Hcy-induced apoptosis and inhibit the effect of Hcy on HUVECs. Furthermore, HSP27 could increase the ratio of Bcl-2/Bax and inhibit caspase-3 activity. Conclusions. Therefore, we concluded that HSP27 played a protective role against Hcy-induced endothelial apoptosis through modulation of ROS production and the mitochondrial caspase-dependent apoptotic pathway.
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