Remote Ischemic Post-Conditioning (RIC) Mediates Anti-Inflammatory Signaling via Myeloid AMPKα1 in Murine Traumatic Optic Neuropathy (TON).

Document Type

Article

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

Keywords

Animals, Mice, AMP-Activated Protein Kinases, Signal Transduction, Optic Nerve Injuries, Mice, Knockout, Ischemic Postconditioning, Male, Mice, Inbred C57BL, Macrophages, Disease Models, Animal, Female, Myeloid Cells, Retinal Ganglion Cells, Transcription Factor Brn-3A

Medical Subject Headings

Animals; Mice; AMP-Activated Protein Kinases; Signal Transduction; Optic Nerve Injuries; Mice, Knockout; Ischemic Postconditioning; Male; Mice, Inbred C57BL; Macrophages; Disease Models, Animal; Female; Myeloid Cells; Retinal Ganglion Cells; Transcription Factor Brn-3A

Publication Date

12-19-2024

Publication Title

Int J Mol Sci

ISSN

1422-0067

Volume

25

Issue

24

PubMed ID

39769388

Digital Object Identifier (DOI)

10.3390/ijms252413626

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