Different types of cell death in vascular diseases

Saberianpour, Shirin; Karimi, Abbas; Modaghegh, Mohammad Hadi Saeed; Ahmadi, Mahdi

doi:10.1007/s11033-021-06402-0

Cited by 6 publications

(2 citation statements)

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“…There are various explanations for the mechanism of cell pathological damage and angiogenesis in cerebral ischemia reperfusion at present (Jurcau & Simion, 2021). The occurrence of cell necrosis and apoptosis is the pathological result of the interaction of receptors and signal pathways at the molecular biological level (Saberianpour et al., 2021). Angiogenesis is also a complex and strictly controlled process (Hatakeyama et al., 2020).…”

Section: Discussionmentioning

confidence: 99%

“…This is called cerebral ischemia‐reperfusion injury (CIRI) (Sharma et al., 2020). Endothelial cells (ECs) are the primary constituents of the blood‐brain barrier, and their dysfunction and death contribute significantly to the pathological progression of CIRI (Li et al., 2020a,b; Zhang et al., 2021; Saberianpour et al., 2021; Nemcovsky et al., 2019; Nitzsche et al., 2021). Although CIRI is a complex pathological process involving multiple cytokines and signaling pathways, it is a deterioration of brain tissue that can be partially repaired through interventions (Khamchai et al., 2022; Tuo et al., 2022).…”

Section: Introductionmentioning

confidence: 99%

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Electroacupuncture reverses endothelial cell death and promotes angiogenesis through the VEGF/Notch signaling pathway after focal cerebral ischemia‐reperfusion injury

et al. 2023

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Background Angiogenesis is an important mechanism of recovery from ischemic stroke. Recent studies have found that there is a close relationship between the VEGF/Notch pathway and angiogenesis. It is unknown whether EA can exert a brain protection effect and promote angiogenesis by acting on the VEGF/Notch signaling pathway after focal cerebral ischemia‐reperfusion injury (CIRI). Methods The Middle Cerebral Artery occlusion/Reperfusion (MCAo/R) model was established, in which rats were subjected to occlusion with ischemic intervention for 30 min, followed by reperfusion for 8 h, 1 day, 3 days, and 7 days. The first EA treatment was performed 90 min after the animal model was successfully established, and then EA treatments were performed once a day for 7 days. The 2,3,5‐triphenyltetrazolium chloride staining and neurological deficit examination were performed to assess the level of CIRI and neuroprotection by EA. Expression levels of VEGFA, Notch1, and Hes1 proteins were measured via western blotting, while the morphological changes of ECs and microvasculature in the cortex were determined using an ultrastructural observation method. Results EA treatment of PC6, GV26, and SP6 can significantly improve the neurological function of MCAO/R rats, reduce the volume of cerebral infarction, and modulate the ultrastructure of ECs and microvessels in pathological states. Western blotting revealed that EA increased VEGFA protein expression at 8 h and 3 days after CIRI, as well as Notch1 protein expression at 1 and 7 days. Subsequently, EA activated the VEGF/Notch pathway, increasing the expression of the downstream target protein Hes1, reversing EC death, and promoting angiogenesis. Conclusion Our findings showed that EA plays a role in promoting angiogenesis following focal CIRI, and we hypothesized that this was due to the regulation of ECs by the EA‐activated VEGF/Notch signaling pathway.

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Section: Discussionmentioning

confidence: 99%