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Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.

Lillian Schulz1, Abby E Young1, Fang Liu2

  • 1Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 13, 2025
PubMed
Summary

Blocking atypical p38 signaling in mice reduced retinal damage and pathological blood vessel growth in oxygen-induced retinopathy. This suggests a new therapeutic target for vascular retinopathies.

Keywords:
Tab1angiogenesisatypical p38oxygen‐induced retinopathyretina

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Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Vascular Biology

Background:

  • Vascular retinopathies affect millions globally, with anti-VEGF therapies offering limited solutions.
  • Mitogen-activated protein kinase (MAPK) p38 signaling is crucial for vascular homeostasis and disease, but atypical pathways remain unexplored in retinopathy.
  • Atypical p38 signaling, mediated by TAB1, regulates inflammation and vascular integrity.

Purpose of the Study:

  • To investigate the role of atypical p38 signaling in oxygen-induced retinopathy (OIR).
  • To explore the therapeutic potential of inhibiting atypical p38 signaling in a mouse model of OIR.

Main Methods:

  • Utilized a genetic knock-in mouse model (Tab1KI) to block atypical p38 activity.
  • Induced oxygen-induced retinopathy (OIR) in Tab1KI and wild-type mice.
  • Performed retinal RNA sequencing (RNAseq) to analyze transcriptional changes.

Main Results:

  • Tab1KI mice showed significantly reduced vaso-obliteration and neovascularization compared to controls.
  • Suppression of atypical p38 altered transcriptional profiles, reducing Mef2c signaling.
  • Reduced Mef2c signaling led to increased microglial activation and inflammation, but decreased pathological angiogenesis while promoting physiological vascular regrowth.

Conclusions:

  • Selective inhibition of atypical p38 signaling effectively reduces pathological neovascularization in OIR without hindering blood vessel repair.
  • Atypical p38 signaling, via Mef2c, plays a critical role in regulating pathological angiogenesis in vascular retinopathies.
  • Targeting atypical p38 offers a promising new therapeutic strategy for treating vascular retinopathies.