ArticleCellular and molecular life sciences : CMLS2025
Acetyl-CoA synthetase 2 alleviates brain injury following cardiac arrest by promoting autophagy in brain microvascular endothelial cells.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- ACSS2-KAT5 complex-driven histone crotonylation orchestrates a pro-inflammatory program to promote the transition from MASLD to MASH.Nature communications · 2026Article
- AAV Vector-Mediated Modulation of Signaling Pathways in Neurological Disorders: Insights From Cellular, Animal, and Human Studies.Cell biochemistry and function · 2026Review
- Identifying therapeutic target genes for stroke through systematic druggable Mendelian randomization analysis.Medicine · 2026Article
- Metabolism-Mediated Regulation of Brain-Heart Interactions.International journal of molecular sciences · 2026Review
- Exogenous lactate administration alleviates post-cardiac arrest brain injury by coordinating metabolic reprogramming and pathological mitophagy suppression.Cellular and molecular life sciences : CMLS · 2026Article
- IL-25-ILC2-IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity.Journal of neuroinflammation · 2026Article
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
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12 authors.
Funding
Abstract
introductionBrain injury is a common sequela following cardiac arrest (CA), with up to 70% of hospitalized patients dying from it. Brain microvascular endothelial cells (BMVECs) play a crucial role in post-cardiac arrest brain injury (PCABI). However, the effects and mechanisms of targeting BMVEC energy metabolism to mitigate brain injury remain unclear.
methodsWe established a mouse model of cardiac arrest by injecting potassium chloride into the right internal jugular vein. Mass spectrometry detected targeted changes in short-chain fatty acids and energy metabolism metabolites in the CA/CPR group compared to the sham group. Mice with overexpressed ACSS2 in BMVECs were created using an AAV-BR1 vector, and ACSS2 knockout mice were generated using the CRE-LOXP system. The oxygen glucose deprivation/re-oxygenation (OGD/R) model was established to investigate the role and mechanisms of ACSS2 in endothelial cells in vitro.
resultsMetabolomics analysis revealed disrupted cerebral energy metabolism post-CA/CPR, with decreased acetyl-CoA and amino acids. Overexpression of ACSS2 in BMVECs increased acetyl-CoA levels and improved neurological function. Vascular endothelial cell-specific ACSS2 knockout mice exhibited reduced aortic sprouting in vitro. Overexpression of ACSS2 improved endothelial dysfunction following oxygen glucose deprivation/re-oxygenation (OGD/R) and influenced autophagy by interacting with transcription factor EB (TFEB) and modulating the AMP-activated protein kinase α (AMPKα) pathway.
conclusionOur study shows that ACSS2 modulates the biological functions of BMVECs by promoting autophagy. Enhancing energy metabolism via ACSS2 may target PCABI treatment development.
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