Oxidative stress drives vascular smooth muscle cell damage in acute Stanford type A aortic dissection through HIF-1α/HO-1 mediated ferroptosis

Song, Wenyu; Chen, Yifu; Qin, Lieyang; Xu, Xinyuan; Sun, Yu; Zhong, Mingzhu; Lu, Yuntao; Hu, Kui; Wei, Lai; Chen, Jinmiao

doi:10.1016/j.heliyon.2023.e22857

Cited by 10 publications

(2 citation statements)

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“…HO-1 accelerates erastin-induced ferroptotic death in fibrosarcoma cells [51]. Induction of ferroptosis by the HIF-1α/HO-1 pathway has been reported in various cells, including neuronal and vascular smooth muscle cells [19][20][21]. Ferroptosis aggravated diabetic nephropathy and damaged renal tubules via the HIF-1α/HO-1 pathway in a mouse model of diabetes [53].…”

Section: Ferroptosismentioning

confidence: 94%

“…HIF-1α stabilization during mild hypoxia may enhance cell regeneration (i.e., angiogenesis and neurogenesis), mitochondrial biogenesis, and cell survival in the brain through HIF-1α target genes [16,17]. In severe hypoxia, HIF-1α causes various gene expression changes and post-translational modifications related to cell damage, mitochondrial dysfunction, cellular lipid peroxidation, and inflammasome formation [18][19][20][21][22] (Figure 1). Here, this review focuses on the detrimental effects of HIF-1α on cell damage under severe hypoxic conditions.…”

Section: Introductionmentioning

confidence: 99%

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Detrimental Roles of Hypoxia-Inducible Factor-1α in Severe Hypoxic Brain Diseases

Choi

2024

IJMS

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Hypoxia stabilizes hypoxia-inducible factors (HIFs), facilitating adaptation to hypoxic conditions. Appropriate hypoxia is pivotal for neurovascular regeneration and immune cell mobilization. However, in central nervous system (CNS) injury, prolonged and severe hypoxia harms the brain by triggering neurovascular inflammation, oxidative stress, glial activation, vascular damage, mitochondrial dysfunction, and cell death. Diminished hypoxia in the brain improves cognitive function in individuals with CNS injuries. This review discusses the current evidence regarding the contribution of severe hypoxia to CNS injuries, with an emphasis on HIF-1α-mediated pathways. During severe hypoxia in the CNS, HIF-1α facilitates inflammasome formation, mitochondrial dysfunction, and cell death. This review presents the molecular mechanisms by which HIF-1α is involved in the pathogenesis of CNS injuries, such as stroke, traumatic brain injury, and Alzheimer’s disease. Deciphering the molecular mechanisms of HIF-1α will contribute to the development of therapeutic strategies for severe hypoxic brain diseases.

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