Cardiolipin-Mediated Alleviation of Mitochondrial Dysfunction Is a Neuroprotective Effect of Statin in Animal Model of Ischemic Stroke

Abstract

In clinical settings, the benefit of statin for stroke is debatable as regular statin users may suffer from myalgia, statin-associated myopathy (SAM), and rarely rhabdomyolysis. Studies suggest that patients on statin therapy show lesser vulnerability toward ischemic stroke and post-stroke frailty. Both pre- and post-treatment benefits of statin have been reported as evident by its neuroprotective effects in both cases. As mitochondrial dysfunction following stroke is the fulcrum for neuronal death, we hereby explore the role of statin in alleviating mitochondrial dysfunction by regulating the mitochondrial dynamics. In the present study, we intend to evaluate the role of statin in modulating cardiolipin-mediated mitochondrial functionality and further providing a therapeutic rationale for repurposing statins either as preventive or an adjunctive therapy for stroke.

Ischemic stroke pathophysiology: A bibliometric and visualization analysis from 1990 to 2022

“…7 , “tissue plasminogen activator” and “acute stroke” were the keywords with the earliest citation outbreaks, which represent the initial status of two keywords in ischemic stroke research [ 53 ]. From 2016 to 2022, the second stage, the citation bursts of keywords, such as “endothelial cell”, “blood brain barrier”, “neuroprotective effect”, “blood-brain barrier”, “inflammation”, “cognitive dysfunction” and “mitochondrial dysfunction” reflect the potential in these directions, focus on basic experiments as well as molecular biology mechanism studies [ [54] , [55] , [56] , [57] , [58] ]. Additionally, “mechanism”, “signaling pathway”, “underlying mechanism”, “leading cause” and “positive effect” are also citation bursts keywords related to mechanisms that have been widely concerned by scholars in recent years [ 59 , 60 ].…”