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<p>Acute cerebral infarction (ACI) is a severe cerebrovascular disease characterized by a steadily rising global incidence rate, emerging as a leading cause of disability and mortality worldwide. Hypoxia-inducible factors (HIFs) play a pivotal role in the pathophysiological process of ACI. In recent years, mounting evidence has suggested a potential interplay between vitamin D (Vit D) and HIFs. Preclinical studies (e.g., rat cerebral ischemia models) have demonstrated that Vit D can stabilize HIF-1α, a key member of the HIFs family, which in turn reduces cerebral infarct volume by up to 50%. Clinical studies (patient cohort follow-ups) further reveal that ACI patients with Vit D-deficiency face a 30% higher risk of poor outcomes. Based on these findings, this review proposes a core hypothesis: Vit D exerts a neuroprotective effect in ACI by modulating HIFs’-related mechanisms, providing a novel direction for disease treatment. We speculate that for Vit D-deficient ACI patients, initiating supplementation therapy (e.g., 6000 IU/day) within 72&#xa0;h ofn onset can reduce infarct volume by ≥ 40% by enhancing the protective effects of HIFs. In summary, the Vit D-HIFs axis is a highly promising therapeutic target for ACI, and future research should focus on validating this mechanism and promoting its clinical translation.</p>

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Vitamin D and hypoxia-inducible factors signaling interplay: A hypothesis-driven review of therapeutic strategies for acute cerebral infarction

  • 期刊论文

  • 发表日期：

    2026年3月18日

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  • Xuan Yan,
  • Zhi-ying Zeng,
  • Shi-xue Dai,
  • Tao Zeng

摘要

Acute cerebral infarction (ACI) is a severe cerebrovascular disease characterized by a steadily rising global incidence rate, emerging as a leading cause of disability and mortality worldwide. Hypoxia-inducible factors (HIFs) play a pivotal role in the pathophysiological process of ACI. In recent years, mounting evidence has suggested a potential interplay between vitamin D (Vit D) and HIFs. Preclinical studies (e.g., rat cerebral ischemia models) have demonstrated that Vit D can stabilize HIF-1α, a key member of the HIFs family, which in turn reduces cerebral infarct volume by up to 50%. Clinical studies (patient cohort follow-ups) further reveal that ACI patients with Vit D-deficiency face a 30% higher risk of poor outcomes. Based on these findings, this review proposes a core hypothesis: Vit D exerts a neuroprotective effect in ACI by modulating HIFs’-related mechanisms, providing a novel direction for disease treatment. We speculate that for Vit D-deficient ACI patients, initiating supplementation therapy (e.g., 6000 IU/day) within 72 h ofn onset can reduce infarct volume by ≥ 40% by enhancing the protective effects of HIFs. In summary, the Vit D-HIFs axis is a highly promising therapeutic target for ACI, and future research should focus on validating this mechanism and promoting its clinical translation.