Deciphering mitochondrial dysfunction: Pathophysiological mechanisms in vascular cognitive impairment
- PMID: 38599056
- DOI: 10.1016/j.biopha.2024.116428
Deciphering mitochondrial dysfunction: Pathophysiological mechanisms in vascular cognitive impairment
Abstract
Vascular cognitive impairment (VCI) encompasses a range of cognitive deficits arising from vascular pathology. The pathophysiological mechanisms underlying VCI remain incompletely understood; however, chronic cerebral hypoperfusion (CCH) is widely acknowledged as a principal pathological contributor. Mitochondria, crucial for cellular energy production and intracellular signaling, can lead to numerous neurological impairments when dysfunctional. Recent evidence indicates that mitochondrial dysfunction-marked by oxidative stress, disturbed calcium homeostasis, compromised mitophagy, and anomalies in mitochondrial dynamics-plays a pivotal role in VCI pathogenesis. This review offers a detailed examination of the latest insights into mitochondrial dysfunction within the VCI context, focusing on both the origins and consequences of compromised mitochondrial health. It aims to lay a robust scientific groundwork for guiding the development and refinement of mitochondrial-targeted interventions for VCI.
Keywords: Calcium homeostasis; Chronic cerebral hypoperfusion; Mitochondria; Oxidative stress; Vascular cognitive impairment; mitophagy.
Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Declaration of competing interest This manuscript has not been published or presented elsewhere, either in part or in its entirety, and is not currently under consideration by another journal. All authors have approved the content of this paper. There are no conflicts of interest to declare.
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