Editorial: Ocular fibrosis: molecular and cellular mechanisms and treatment modalities

Abstract

Editorial on the Research TopicOcular fibrosis: molecular and cellular mechanisms and treatment modalities Tissue fibrosis occurs as an excessive repair response to mechanical damage, inflammation, ischemia, and degeneration, leading to irreversible scar formation (1). The excessive proliferation and deposition of various extracellular matrix (ECM) proteins are mediated through the transition of various cell types to myofibroblast-like cells. These cell types include epithelial cells, fibroblasts, vascular cells, glial cells, and inflammatory cells (2). The noted phenotypic and functional changes are considered major events during the fibrotic process with severe alterations in the tissue integrity and function (3,4). Fibrosis contributes to the severity of pathologies in many chronic inflammatory diseases in the eye including retinopathy of prematurity, proliferative diabetic retinopathy (PDR), age-related macular degeneration (AMD), and glaucoma (1, 5). Although the mechanisms of fibrogenesis have been extensively studied, the exact molecular and cellular events that drive this destructive tissue insult remain unresolved and may vary in a tissue, cell, and context-dependent manner. Despite great advances in our knowledge regarding its etiology, effective treatment of fibrogenesis presents an unmet challenge.Numerous in vitro and in vivo models of fibrogenesis have helped gain insight into the role of various factors and their impact on intracellular mechanisms that drive the changes associated with fibrotic responses. Unfortunately, targeting many of these cells and pathways has proven ineffective in the prevention and reversal of fibrotic responses in Frontiers in Ophthalmology frontiersin.org 01