Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

28 Feb 2023

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Corneal surgery and disorders
Share to Corneal Surgery and Treatments
Share to Retinopathy of Prematurity Studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36854766
DOI: 10.1038/s41598-023-30383-8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Rescuing cellular function in Fuchs endothelial corneal dystrophy by healthy exogenous mitochondrial internalizationPMID 36854766Read ↗

Mitochondrial Dysfunction and Mitophagy in Fuchs Endothelial Corneal DystrophySemantic proximity Read ↗

Endoplasmic Reticulum-Mitochondria Crosstalk in Fuchs Endothelial Corneal Dystrophy: Current Status and Future ProspectsSemantic proximity Read ↗

Chronology of cellular events related to mitochondrial burnout leading to cell death in Fuchs endothelial corneal dystrophySemantic proximity Read ↗

Mitophagy: An Emerging Target in Ocular PathologySemantic proximity Read ↗

Restoration of Mitochondrial Integrity, Telomere Length, and Sensitivity to Oxidation by In Vitro Culture of Fuchs' Endothelial Corneal Dystrophy CellsSemantic proximity Read ↗

Chronic ER Stress Disrupts Mitochondrial-Associated ER Membrane Integrity in Corneal Endothelial CellsSemantic proximity Read ↗

Role of mitochondrial dysfunction in ocular surface diseasesSemantic proximity Read ↗

Genetic mutations and molecular mechanisms of Fuchs endothelial corneal dystrophySemantic proximity Read ↗

Preclinical Models for Studying Fuchs Endothelial Corneal DystrophySemantic proximity Read ↗

Proteasomal Dysfunction results in ER stress, Endo MT, oxidative stress, and apoptotic cell death resulting in Fuchs Corneal Endothelial Dystrophy like features in miceSemantic proximity Read ↗

SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stressSemantic proximity Read ↗

Fuchs endothelial corneal dystrophy: current perspectivesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.