ArticleNeurochemical research2025
ALDH2 Overexpression Improves the Blood-brain Barrier and Represses Mitochondrial Dysfunction in Chronic Cerebral Hypoperfusion Through the SIRT1/ROS Axis.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Allosteric Activation of GDH/TCA Pathway Reduces Pathological Build-Up and Promotes Neuronal Survival in an In Vitro Model of Alzheimer's Disease.Biomolecules · 2026Article
- Intranasal administration of thermoresponsive pterostilbene loaded nanoemulgel confers neuroprotection in a rat model of ischemic stroke.Nanomedicine (London, England) · 2025Article
- Polygalasaponin F alleviates cerebral ischemia-reperfusion injury through inhibiting mitophagy.Metabolic brain disease · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The study investigated the mechanism of ALDH2 in mitochondrial dysfunction and blood-brain barrier (BBB) damage arising from chronic cerebral hypoperfusion (CCH). A rat model of bilateral common carotid artery occlusion (BCCAO) was established and treated with AAV-ALDH2. ALDH2 expression, cognitive function, and levels of inflammation- and oxidative stress-related factors, were examined, followed by observing changes in BBB and mitochondrial functions. A rat neuron model of oxygen glucose deprivation/re-oxygenation (OGD/R) was constructed and treated with AAV-ALDH2 and the SIRT1 inhibitor Sirtinol. 4-HNE, SIRT1, ROS levels, mitochondrial membrane potential (MMP), and ATP production were detected, followed by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) assays. ALDH2 was down-regulated in BCCAO-modeled rats. In BCCAO-modeled rats, ALDH2 overexpression repressed learning/memory deficits and BBB leakage, elevated SOD and GSH levels, decreased the levels of inflammation-related factors, ROS, 4-HNE, and MDA, and improved mitochondrial morphology. In OGD/R-stimulated neurons, ALDH2 overexpression diminished ROS and 4-HNE levels and ECAR and increased MMP, OCR, and ATP production, which was abrogated by Sirtinol. Overall, ALDH2 up-regulation exerts suppressive effects on BBB damage and mitochondrial dysfunction in CCH via the SIRT1/ROS axis.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.