Microglia activation and migration in retina during acute high-altitude exposure

Yuting Li1, Cong Han2, Jianping Zhang2

  • 1Department of Pathology, Basic Medical School, Ningxia Medical University, Yinchuan, 750004, PR China; Department of Ophthalmology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, 730030, Gansu, PR China.

Experimental Eye Research
|September 25, 2025
PubMed

Insights

High-altitude exposure causes retinal dysfunction by activating microglia, leading to inflammation and edema. This study reveals microglial migration and pro-inflammatory changes are key mechanisms in high-altitude retinopathy.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Immunology

Background:

  • High-altitude retinopathy (HAR) is a retinal dysfunction caused by hypobaric hypoxia.
  • The precise pathogenic mechanisms of HAR, particularly the role of microglia, remain unclear.

Purpose of the Study:

  • To investigate microglial functional alterations and activation mechanisms in a mouse model of high-altitude exposure.
  • To elucidate the role of microglia in retinal edema and functional impairment under hypobaric hypoxia.

Main Methods:

  • Mouse models were exposed to high altitude (5000m HAE).
  • Hematoxylin and eosin (H&E) staining, electroretinogram (ERG) testing, and immunofluorescence staining were performed.
  • Changes in microglial numbers, activation status, Connexin43 (Cx43) immunoreactivity, and interleukin-1β (IL-1β) levels were assessed.

Main Results:

  • High-altitude exposure induced retinal edema and impaired retinal function (ERG).
  • Microglial numbers increased, and activated microglia migrated within the retina during hypoxic injury.
  • Activated microglia showed a shift towards pro-inflammatory subtypes, with increased Cx43 and IL-1β levels.

Conclusions:

  • Microglial activation and migration are integral to retinal edema and functional injury in hypobaric hypoxia.
  • Dynamic changes in Cx43 and elevated IL-1β levels are associated with microglial inflammatory activation during acute high-altitude exposure.