Mitochondrial dysfunction in cerebrovascular diseases: mechanisms and neurological consequences

Mitochondria are central regulators of cellular metabolism, redox balance, and cell survival in the nervous system. In recent years, growing evidence has highlighted mitochondrial dysfunction as a critical contributor to the pathophysiology of cerebrovascular diseases, including ischemic and hemorrhagic stroke, cerebral small vessel disease, and vascular cognitive impairment. Because neurons, astrocytes, microglia, and cerebrovascular endothelial cells have high metabolic demands and tightly regulated mitochondrial dynamics, disturbances in mitochondrial function can profoundly influence neural viability and neurovascular unit integrity during cerebrovascular injury.Cerebrovascular events trigger complex mitochondrial responses involving impaired oxidative phosphorylation, excessive production of reactive oxygen species, calcium dysregulation, altered mitochondrial dynamics, and activation of cell death pathways. These processes contribute not only to acute neuronal injury but also to secondary complications such as neuroinflammation, blood–brain barrier disruption, impaired neurovascular coupling, and long term cognitive decline. Increasing attention has also been given to the role of mitochondrial signaling in post stroke recovery, neuroplasticity, and vascular remodeling.Despite substantial advances, key questions remain regarding how mitochondrial dysfunction develops across different cell types of the neurovascular unit, how these alterations interact with systemic vascular risk factors, and how mitochondrial pathways influence both acute injury and chronic neurological complications following cerebrovascular events. Moreover, translating mechanistic insights into effective therapeutic strategies remains a major challenge.This Research Topic aims to provide an updated overview of mitochondrial mechanisms involved in cerebrovascular diseases and their neurological complications. By integrating findings from molecular neuroscience, cellular studies, experimental models, and translational research, this collection seeks to clarify how mitochondrial dysfunction contributes to cerebrovascular pathology and to identify potential mitochondrial targets for neuroprotective and neurorestorative therapies.We welcome original research articles, reviews, and perspectives addressing topics including, but not limited to:o Mitochondrial dysfunction in ischemic and hemorrhagic strokeo Mitochondrial regulation of the neurovascular unit during cerebrovascular injuryo Oxidative stress, mitochondrial dynamics, and mitophagy in cerebrovascular pathologyo Mitochondrial contributions to blood–brain barrier disruption and neuroinflammationo Mitochondrial mechanisms underlying post stroke cognitive impairment and vascular dementiao Cell type specific mitochondrial responses in neurons, astrocytes, microglia, and endothelial cellso Interactions between mitochondrial dysfunction and vascular risk factors (e.g., aging, hypertension, diabetes)o Mitochondria targeted therapeutic strategies in cerebrovascular diseaseso Mitochondrial biomarkers and imaging approaches in stroke and cerebrovascular disordersBy focusing on mitochondrial mechanisms within cerebrovascular disease processes, this Research Topic aims to advance current understanding of how mitochondrial dysfunction shapes neurological outcomes and to stimulate new approaches for diagnosis, prevention, and treatment. Topic editors: Ganna Nevoit, Gediminas Jaruševičius Source: https://www.frontiersin.org/research-topics/78992/mitochondrial-dysfunction-in-cerebrovascular-diseases-mechanisms-and-neurological-consequences