Изменения митохондриальной ДНК в фибробластах и миофибробластах роговицы после повреждения

Alterations in Mitochondrial DNA in Corneal Fibroblast and Myofibroblast Post Injury.

Corneal myofibroblasts (CMFs) are the major facilitators of corneal tissue repair after injury, trauma, or infection.^1,2 CMFs are generated from keratocytes/fibroblasts (corneal stromal fibroblasts [CSFs]), the resident cells of the corneal stroma, after injury under influence of transforming growth factor beta-1 (TGFβ1) and other growth factors in the cornea.³ Although formation of CMFs is paramount for corneal wound healing, their excessive formation and persistence in stroma after wound closure result in scarring and vision impairment.⁴ Unlike CSFs, CMFs are characterized by a significant increase in α-smooth muscle actin (αSMA) levels, the ability to enhance extracellular matrix (ECM) protein production, low optical density, and high metabolic activity.^5,6 These CMF properties prompted us to postulate that mitochondria in CSFs undergo significant modifications during transdifferentiation to CMFs to meet increased energy demands for sustaining newly attained contractile phenotype and function by increasing aerobic glycolysis and oxidative phosphorylation during corneal wound healing. Also, mitochondrial biogenesis and mitophagy play a key role in proper CMF functioning.