Rescuing cellular function in Fuchs endothelial corneal dystrophy by healthy exogenous mitochondrial internalization.

ABSTRACT: Fuchs endothelial corneal dystrophy (FECD) is characterized by an accelerated loss of corneal endothelial cells. Since the function of these cells is to maintain the cornea in a state of deturgescence necessary for its transparency, the depletion of corneal endothelial cells ultimately causes corneal edema and irreversible loss of vision. Evidence is accumulating regarding the central involvement of mitochondria in FECD. As we have previously shown, when endothelial cells die and are not replaced, the mitochondria of surviving cells must provide more energy to compensate, leading to a phenomenon we have called mitochondrial burnout. This burnout causes cell death, thus exacerbating an irreversible vicious circle responsible for FECD progression. Corneal transplantation, for which the trans

SUBMITTER: Methot S 

PROVIDER: S-EPMC9974992 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature