ArticleInternational journal of molecular sciences2024
Remote Ischemic Post-Conditioning (RIC) Mediates Anti-Inflammatory Signaling via Myeloid AMPKα1 in Murine Traumatic Optic Neuropathy (TON).
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- IL-34 Regulates Macrophage Polarization and Bone Defect Healing in Aged Mice.International journal of molecular sciences · 2026Article
- Innate lymphoid cells: unsung heroes or villains in multiple sclerosis pathogenesis?Immunologic research · 2026Review
- Dual immune armies in glaucoma: microglia and monocyte-derived macrophages.Frontiers in immunology · 2026Review
- N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment.Cell death discovery · 2025Review
- Immuno-nutritional therapy in experimental autoimmune encephalomyelitis: a translational pathway to multiple sclerosis management.Inflammopharmacology · 2025Review
- Aquaporin-4 triggers inflammation in a murine endotoxin-induced uveitis (EIU) model.BMC ophthalmology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Traumatic optic neuropathy (TON) has been regarded a vision-threatening condition caused by either ocular or blunt/penetrating head trauma, which is characterized by direct or indirect TON. Injury happens during sports, vehicle accidents and mainly in military war and combat exposure. Earlier, we have demonstrated that remote ischemic post-conditioning (RIC) therapy is protective in TON, and here we report that AMPKα1 activation is crucial. AMPKα1 is the catalytic subunit of the heterotrimeric enzyme AMPK, the master regulator of cellular energetics and metabolism. The α1 isoform predominates in immune cells including macrophages (Mφs). Myeloid-specific AMPKα1 KO mice were generated by crossing AMPKα1
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