ArticleArchives of medical science : AMS2026
Overexpression of PGC-1α reduces inflammation and protects against focal cerebral ischaemia/reperfusion injury.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- SIRT1/AMPK/PGC1α pathway in ischemic stroke: Elucidating neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Systemic nicotinamide mononucleotide administration to mitigate post-cardiac arrest brain injury in mice.PloS one · 2025Article
- Novel Therapeutic Approaches Enhance PGC1-alpha to Reduce Oxidant Stress-Inflammatory Signaling and Improve Functional Recovery in Hibernating Myocardium.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Cerebral ischaemia and subsequent reperfusion can cause brain damage. Herein we investigate the impact of PGC-1α expression following I/R injury with overexpressed PGC-1α versus wild-type mice. Material and methods: Focal cerebral I/R was performed in the wild-type and transgenic mouse models. In both mouse groups we evaluated the redox status by measuring reactive oxygen species (ROS) content, infarct volumes, neurological scoring, protein (western blot analysis), and cytokine (enzyme-linked immunosorbent assay) expression. Results: The results showed that PGC-1α expression was significantly down-regulated in I/R injury compared to the sham mice. I/R injury increased ROS levels and further up-regulated apoptosis. PGC-1α-overexpressed mice down-regulated I/R injury-induced neurological deficit scores and infarct volume. In addition, compared to WT mice during I/R injury, PGC-1α-overexpressed mice significantly down-regulated inflammatory proteins (NF-κB, COX-2, NLRP3) and cytokine (TNF-α, IL-1β, IL-6) expressions. I/R injured mice showed severe decline in Nrf-2, HO-1, and NQO1 expressions. Conclusions: Importantly, PGC-1α/Nrf-2 suppression during cerebral I/R injury causes overall brain damage through increased oxidative stress, neuro-inflammation, and apoptosis. PGC-1α-overexpressed mice promoted cytoprotection through Nrf-2 regulation during cerebral ischaemia/reperfusion (I/R) injury. Thus, PGC-1α overexpression leads to lesser injury following ischaemia, thereby preserving mitochondrial activity. PGC-1α might act as therapeutic target protein and thereby protect against cerebral damage during I/R injury.
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