FGF23与缺血性脑卒中的关系及其相关 生物学机制
The Relationship between FGF23 and Ischemic Stroke and Related Biological Mechanisms
DOI: 10.12677/acm.2026.1652110, PDF,   
作者: 杨采妮, 李 迅:西安医学院研究生工作部,陕西 西安;毕 皎, 李雪萍*:西安医学院临床医学院,西安常见老年病防治重点实验室,陕西 西安
关键词: FGF23缺血性脑卒中血管内皮功能动脉粥样硬化FGF23 Ischemic Stroke Vascular Endothelial Function Atherosclerosis
摘要: 缺血性脑卒中是一种因颅内和颈动脉粥样硬化导致血流中断引发的脑组织损伤的疾病,已成为我国乃至全球成年人致死致残的最主要原因之一。成纤维细胞生长因子23 (Fibroblast growth factor 23, FGF23)是一种骨源性激素,其功能是抑制肾脏磷酸盐再吸收和维生素D合成,参与维持机体钙磷代谢平衡,病理条件下与心脑血管疾病密切相关。研究提示FGF23水平升高会影响血管内皮功能,加剧动脉粥样硬化和血管钙化程度,进而加速缺血性脑卒中的发生发展过程。因此,FGF23作为缺血性脑卒中潜在的预测因子及治疗靶点引起广泛关注,本文就FGF23对缺血性脑卒中的影响及相关生物学机制进行综述,以期为临床治疗和预防缺血性脑卒中带来新思路。
Abstract: Ischemic stroke (IS), a brain tissue injury characterized by the interruption of blood flow due to intracranial and carotid atherosclerosis, has become one of the leading causes of death and disability among adults both in China and worldwide. Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that suppresses renal phosphate reabsorption and vitamin D synthesis, thereby maintaining systemic calcium-phosphate homeostasis, and FGF23 is closely linked to cardiovascular and cerebrovascular diseases under pathological conditions. Emerging evidence indicated that elevated levels of FGF23 could impair vascular endothelial function, exacerbate atherosclerosis and vascular calcification, consequently accelerating the onset and progression of IS. Thus, FGF23 has attracted widespread attention as a potential predictive biomarker and therapeutic target for IS, this review summarized the influence of FGF23 on IS and its underlying biological mechanisms, aiming to provide novel insights for the clinical prevention and treatment of IS.
文章引用:杨采妮, 李迅, 毕皎, 李雪萍. FGF23与缺血性脑卒中的关系及其相关 生物学机制[J]. 临床医学进展, 2026, 16(5): 2968-2973. https://doi.org/10.12677/acm.2026.1652110

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