A Tale of Two: When Neural Stem Cells Encounter Hypoxia

Fan, Yiting; Li, Jinshi; Fang, Bo

doi:10.1007/s10571-022-01293-6

Cited by 4 publications

(2 citation statements)

References 193 publications

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“…It is known that normobaric hypoxia activates synthetic and proliferative activity in cells [103], and a number of recent experimental studies have shown that hypoxic preconditioning enhances the proliferative activity of mesenchymal stem cells [104,105], as well as neural stem cells [106].…”

Section: Proliferative and Synthetic Activitymentioning

confidence: 99%

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Tregub,

Kulikov,

Ibrahimli

et al. 2024

IJMS

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The review introduces the stages of formation and experimental confirmation of the hypothesis regarding the mutual potentiation of neuroprotective effects of hypoxia and hypercapnia during their combined influence (hypercapnic hypoxia). The main focus is on the mechanisms and signaling pathways involved in the formation of ischemic tolerance in the brain during intermittent hypercapnic hypoxia. Importantly, the combined effect of hypoxia and hypercapnia exerts a more pronounced neuroprotective effect compared to their separate application. Some signaling systems are associated with the predominance of the hypoxic stimulus (HIF-1α, A1 receptors), while others (NF-κB, antioxidant activity, inhibition of apoptosis, maintenance of selective blood–brain barrier permeability) are mainly modulated by hypercapnia. Most of the molecular and cellular mechanisms involved in the formation of brain tolerance to ischemia are due to the contribution of both excess carbon dioxide and oxygen deficiency (ATP-dependent potassium channels, chaperones, endoplasmic reticulum stress, mitochondrial metabolism reprogramming). Overall, experimental studies indicate the dominance of hypercapnia in the neuroprotective effect of its combined action with hypoxia. Recent clinical studies have demonstrated the effectiveness of hypercapnic–hypoxic training in the treatment of childhood cerebral palsy and diabetic polyneuropathy in children. Combining hypercapnic hypoxia with pharmacological modulators of neuro/cardio/cytoprotection signaling pathways is likely to be promising for translating experimental research into clinical medicine.

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Section: Proliferative and Synthetic Activitymentioning

confidence: 99%

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Tregub,

Kulikov,

Ibrahimli

et al. 2024

IJMS

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show abstract

“…[29]. It is present in numerous diseases, such as in atherosclerosis, where an imbalance between oxygen supply and demand results in high-fat arterial wall lesions and plaque formation, increased lipid accumulation, and inflammatory responses[6][7][8].…”

mentioning

confidence: 99%

Hypoxia-mediated SUMOylation of FADD exacerbates endothelial cell injury via the RIPK1-RIPK3-MLKL sig-naling axis

Yu,

Yang,

Wen

et al. 2024

Preprint

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Vascular endothelial cells are the predominant cell type in the cardiovascular system, and endothelial dysfunction and death fol-lowing hypoxic injury lead to vascular lesions and play an essential role in the progression of cardiovascular disease. However, the mechanisms and specific interventions of vascular endothelial cell injury under hypoxia remain unclear. Here, we reported that hypox-ia induces the development of necroptosis and exacerbates in-flammatory injury in vascular endothelial cells in vivo and in vitro. We identified FADD as a critical regulator of hypoxia-mediated necroptosis, and the knockdown of FADD effectively reversed hy-poxia-induced necroptosis. Mechanistically, hypoxia affected pro-tein conformation through SUMOylation of FADD and competitively inhibited its ubiquitination, leading to an increase in protein half-life and protein level of FADD. On the other hand, SUMOylation in-creased the interaction between FADD and RIPK1 and induced the formation of the FADD-RIPK1-RIPK3 complex, thereby promoting necroptosis in vascular endothelial cells. The SUMOylation inhibi-tor ginkgolic acid (GA) notably reduced hypoxia-induced vascular endothelial injury and inflammatory responses in male mice. Take together, our research has uncovered a new process by which SUMOylation of FADD controls the occurrence of hypoxia-induced necroptosis in endothelial cells, which could identify new therapeu-tic targets for hypoxia-induced diseases.

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Hypoxia preconditioning increases Notch1 activity by regulating DNA methylation in vitro and in vivo

Chang,

Liu,

Fan

et al. 2024

Mol Biol Rep

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A Tale of Two: When Neural Stem Cells Encounter Hypoxia

Cited by 4 publications

References 193 publications

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia

Hypoxia-mediated SUMOylation of FADD exacerbates endothelial cell injury via the RIPK1-RIPK3-MLKL sig-naling axis

Hypoxia preconditioning increases Notch1 activity by regulating DNA methylation in vitro and in vivo

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