内质网-线粒体互作在卒中后认知障碍中的研究进展

doi:10.3969/j.issn.1006-5725.2024.07.025

Abstract

Abstract:

Post-stroke cognitive impairment （PSCI），refers to a range of clinical syndromes of cognitive impairment caused by stroke. Although its specific pathogenesis is still unclear，many studies have confirmed that endoplasmic reticulum-mitochondria interaction has become a key hub for intracellular signal transduction and substance metabolism， and its regulation of various biological processes，such as Ca²⁺ balance，lipid metabolism，mitochondrial dynamics，autophagy， and neuroinflammation，is closely related to the development of PSCI. Therefore，in this paper，we will review the various functions of endoplasmic reticulum-mitochondrial interactions and explore their specific roles in PSCI，in order to discover new therapeutic targets and provide new theoretical basis and references for the development of PSCI-targeted drugs in the future.

Key words: stroke, cognitive impairment, endoplasmic reticulum mitochondrial interactions, mitochondrial dynamics, autophagy, review

CLC Number:

R743.33

Lulu CHEN,Meng LUO,Kaiqi SU,Jing GAO,Xiaodong. FENG. Research progress of the endoplasmic reticulum⁃mitochondrial interactions in post⁃stroke cognitive impairment[J]. The Journal of Practical Medicine, 2024, 40(7): 1023-1028.

Figures/Tables 2

References 45

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内质网-线粒体互作的生物学功能	相关蛋白	具体作用	参考文献
Ca⁺运输	VDAC1	线粒体的钙摄取通道	［16］
	IP3R	内质网的钙释放通道
	Grp75	连接线粒体外膜上的VDAC1与内质网上的IP3R，介导两者间的钙转移
	VAPB/PTPIP51	连接内质网与线粒体介导两者间的钙转移	［42］
	Sig-1R	可延长从内质网到线粒体的Ca²⁺信号传导	［12］
脂质代谢	PSS	催化磷脂酰丝氨酸合成的关键酶	［24］
脂质代谢	ACAT1	催化游离胆固醇转化为胆固醇酯	［25］
线粒体动力学	OPA1	参与线粒体内膜的融合	［27］
	Mfn2	参与线粒体外膜的融合	［27］
	Drp1	线粒体分裂的启动蛋白	［29］
	Fis1	与Drp1协作共同参与线粒体分裂	［29］
自噬	Beclin1	自噬形成的关键蛋白	［37］
	ATG5/9/14	调节自噬前体的形成并作为自噬标记物	［38］
	Stx17	与ATG14相互作用，参与自噬小体的形成	［39］
	PINK1/Parkin	介导线粒体自噬	［40］
炎症	NLRP3	形成多分子NIRP3炎性复合体介导炎症的发生	［45］

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Research progress of the endoplasmic reticulum⁃mitochondrial interactions in post⁃stroke cognitive impairment

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