Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.

ABSTRACT: Despite the life-changing impact of anti-VEGF therapies, vascular retinopathies continue to affect millions of patients worldwide. To better understand disease progression, it is essential to define alternative mechanisms that contribute to retinal vascular dysregulation. Mitogen-activated protein kinase (MAPK) p38 plays a significant role in regulating vascular homeostasis, angiogenesis, and retinal disease progression, yet effective therapeutic targeting remains elusive. An alternative atypical p38 signaling pathway is mediated by interaction with the adaptor protein TGF-beta activated kinase 1, binding protein 1 (TAB1). Atypical p38 can be activated by ischemia or by inflammatory G protein-coupled receptors (GPCRs) to regulate inflammation and vascular homeostasis. However, atypical sig

SUBMITTER: Schulz L 

PROVIDER: S-EPMC12701566 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature