What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review

Lou, Xiaokun; Zhang, Yuanyuan; Guo, Jianchun; Gao, Lijie; Ding, Yingying; Zhuo, Xiaohui; Lei, Qingqing; Bian, Jing; Lei, Ruiting; Gong, Wenyan; Zhang, Xingwei; Jiao, Qibin

doi:10.1007/s10741-023-10336-z

Cited by 10 publications

(2 citation statements)

References 146 publications

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“…Our investigation into the impact of kaempferol on lipid peroxidation, utilizing assays like DHE for intracellular ROS levels 30 and C11-BODIPY for lipid peroxidation 40 , confirmed significant inhibition of RSL3-induced lipid peroxidation in HUVECs. Multiple regulatory signals such as GPX4 and SLC7A11 are involved in the regulation of cell ferroptosis 54 . The GSH-GPX4 limits membrane lipid peroxidation via targeting System Xc¯cystine/glutamate antiporter 55, 56 .…”

Section: Discussionmentioning

confidence: 99%

Kaempferol Rescues Vascular Endothelial Ferroptosis by Inhibiting Lipid Peroxidation

Wen,

Zhang,

Wang

et al. 2024

Biomed. Res. Ther.

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Introduction:The vascular endothelium plays a pivotal role in maintaining vascular function and physiological balance. The degradation and injury of endothelial cells are critical pathological events in the progression of vascular diseases, leading to cell death. One such cell death mechanism, ferroptosis, is an iron-dependent form of necrosis characterized by extensive lipid peroxidation-mediated membrane damage and the toxic effects of iron and lipid peroxidation. Kaempferol, a flavonoid, is celebrated for its antioxidant, anti-inflammatory, and anti-cancer properties. Despite these benefits, the impact of Kaempferol on endothelial cell ferroptosis and its potential therapeutic applications in vascular diseases have yet to be fully elucidated. Methods: Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Oxidative stress and lipid peroxidation were measured using Dihydroethidium (DHE) and C11-BODIPY 581/591, respectively. The protein and RNA levels of ferroptosis-associated molecules, including solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), were determined through Western blotting and real-time fluorescence quantitative polymerase chain reaction (qPCR). Results: Treatment with a glutathione peroxidase 4 inhibitor (RSL3) led to rapid cytotoxicity in human umbilical vein endothelial cells (HUVECs). Notably, Kaempferol demonstrated a significant protective effect against RSL3-induced ferroptosis in HUVECs. Kaempferol treatment reduced the accumulation of reactive oxygen species (ROS) and exhibited distinctive morphological changes associated with ferroptosis. Moreover, Kaempferol treatment resulted in the upregulation of SLC7A11 and GPX4 expression in HUVECs, highlighting its potent ability to mitigate ferroptosis among tested flavonoids. Conclusions: Kaempferol effectively inhibited RSL3-induced ferroptosis in HUVECs by modulating the expression of SLC7A11 and GPX4, thereby reducing lipid peroxidation. These findings underscore the therapeutic potential of Kaempferol in the treatment of vascular diseases, paving the way for its application in clinical settings.

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Section: Discussionmentioning

confidence: 99%

Kaempferol Rescues Vascular Endothelial Ferroptosis by Inhibiting Lipid Peroxidation

Wen,

Zhang,

Wang

et al. 2024

Biomed. Res. Ther.

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“…There is evidence that ferroptosis participates in diabetes-induced cardiomyopathy [120,121]. Streptozotocin induces diabetic cardiomyopathy and ferroptosis in the myocardial tissue of mice [40,75,81,85,122,123].…”

Section: Diabetic Cardiomyopathymentioning

confidence: 99%

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Ryabov,

Maslov,

Vyshlov

et al. 2024

IJMS

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The hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is about 6% and has not decreased in recent years. The leading cause of death of these patients is ischemia/reperfusion (I/R) cardiac injury. It is quite obvious that there is an urgent need to create new drugs for the treatment of STEMI based on knowledge about the pathogenesis of I/R cardiac injury, in particular, based on knowledge about the molecular mechanism of ferroptosis. In this study, it was demonstrated that ferroptosis is involved in the development of I/R cardiac injury, antitumor drug-induced cardiomyopathy, diabetic cardiomyopathy, septic cardiomyopathy, and inflammation. There is indirect evidence that ferroptosis participates in stress-induced cardiac injury. The activation of AMPK, PKC, ERK1/2, PI3K, and Akt prevents myocardial ferroptosis. The inhibition of HO-1 alleviates myocardial ferroptosis. The roles of GSK-3β and NOS in the regulation of ferroptosis require further study. The stimulation of Nrf2, STAT3 prevents ferroptosis. The activation of TLR4 and NF-κB promotes ferroptosis of cardiomyocytes. MiR-450b-5p and miR-210-3p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation through the inhibition of ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-208a/b, miR-375-3p, miR-26b-5p and miR-15a-5p can aggravate myocardial ferroptosis.

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Effect of advanced glycation end-products in a wide range of medical problems including COVID-19

Bronowicka-Szydełko,

Gostomska-Pampuch,

Kuzan

et al. 2024

Advances in Medical Sciences

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What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review

Cited by 10 publications

References 146 publications

Kaempferol Rescues Vascular Endothelial Ferroptosis by Inhibiting Lipid Peroxidation

Kaempferol Rescues Vascular Endothelial Ferroptosis by Inhibiting Lipid Peroxidation

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Effect of advanced glycation end-products in a wide range of medical problems including COVID-19

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