ArticleRedox biology2019
HSP22 suppresses diabetes-induced endothelial injury by inhibiting mitochondrial reactive oxygen species formation.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
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- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Retinoic Acid Improves Vascular Endothelial Dysfunction by Inhibiting PI3K/AKT/YAP-mediated Ferroptosis in Diabetes Mellitus.Current pharmaceutical design · 2025Article
- EndothelialCurrent diabetes reviews · 2025Review
- Induction, amplification, and propagation of diabetic retinopathy-associated inflammatory cytokines between human retinal microvascular endothelial and Müller cells and in the mouse retina.Cellular signalling · 2024Article
- Heat shock protein 22 alleviates doxorubicin-induced kidney injury by suppressing oxidative stress and apoptosis.Scientific reports · 2024Article
- HSPB8 attenuates lipopolysaccharide‑mediated acute lung injury in A549 cells by activating mitophagy.Molecular medicine reports · 2024Article
- The ischemia-enhanced myocardial infarction protection-related lncRNA protects against acute myocardial infarction.MedComm · 2024Article
- Puerarin mitigated LPS-ATP or HG-primed endothelial cells damage and diabetes-associated cardiovascular disease via ROS-NLRP3 signalling.Journal of cellular and molecular medicine · 2024Article
- HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction.Experimental and therapeutic medicine · 2024Article
- Heat Shock Protein 22 Attenuates Nerve Injury-induced Neuropathic Pain Via Improving Mitochondrial Biogenesis and Reducing Oxidative Stress Mediated By Spinal AMPK/PGC-1α Pathway in Male Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Mitochondrial reactive oxygen species promote mitochondrial damage in high glucose-induced dysfunction and apoptosis of human dental pulp cells.Journal of dental sciences · 2024Article
- The role of heat shock proteins in the pathogenesis of heart failure (Review).International journal of molecular medicine · 2023Review
- Review
- Rosiglitazone reduces diabetes angiopathy by inhibiting mitochondrial dysfunction dependent on regulating HSP22 expression.iScience · 2023Article
- Macrophage-specific autophagy-related gene HSPB8 is involved in the macrophage polarization in atherosclerosis.BMC cardiovascular disorders · 2023Article
- HSPB8 Overexpression Ameliorates Cognitive Impairment in Diabetic Mice via Inhibiting NLRP3 Inflammation Activation.Oxidative medicine and cellular longevity · 2022Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction of mitochondrial reactive oxygen species (mtROS) by hyperglycemia is a key event responsible for endothelial activation and injury. Heat shock protein 22 (HSP22) is a stress-inducible protein associated with cytoprotection and apoptosis inhibition. However, whether HSP22 prevents hyperglycemia-induced vascular endothelial injury remains unclear. Here, we investigated whether HSP22 protects the vascular endothelium from hyperglycemia-induced injury by reducing mtROS production. We used a high-fat diet and streptozotocin injection model to induce type 2 diabetes mellitus (T2DM, metabolic syndrome) and exposed human umbilical vein endothelial cells (HUVECs) to high glucose following overexpression or silencing of HSP22 to explore the role of HSP22. We found that HSP22 markedly inhibited endothelial cell activation and vascular lesions by inhibiting endothelial adhesion and decreasing cytokine secretion. We performed confocal microscopy and flow cytometry assays using HUVECs and showed that HSP22 attenuated mtROS and mitochondrial dysfunction in hyperglycemia-stimulated endothelial cells. Mechanistically, using the mtROS inhibitor MitoTEMPO, we demonstrated that HSP22 suppressed endothelial activation and injury by eliminating hyperglycemia-mediated increases in mtROS. Furthermore, we found that HSP22 maintained the balance of mitochondrial fusion and fission by mitigating mtROS in vitro. HSP22 attenuated the development of vascular lesions by suppressing mtROS-mediated endothelial activation in a T2DM mouse model. This study provides evidence that HSP22 may be a promising therapeutic target for vascular complications in T2DM.
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