Abstract
Autophagy is a robust cellular mechanism for disposing of harmful molecules or recycling them to cells, which also regulates physiopathological processes in cornea. Dysregulated autophagy causes inefficient clearance of unwanted proteins and cellular debris, mitochondrial disorganization, defective inflammation, organ dysfunctions, cell death, and diseases. The cornea accounts for two-thirds of the refraction of light that occurs in the eyes, but is prone to trauma/injury and infection. The extracellular matrix (ECM) is a noncellular dynamic macromolecular network in corneal tissues comprised of collagens, proteoglycans, elastin, fibronectin, laminins, hyaluronan, and glycoproteins. The ECM undergoes remodeling by matrix-degrading enzymes and maintains corneal transparency. Autophagy plays an important role in the ECM and wound healing maintenance. Delayed/dysregulated autophagy impacts the ECM and wound healing, and can lead to corneal dysfunction. Stromal wound healing involves responses from the corneal epithelium, basement membrane, keratocytes, the ECM, and many cytokines and chemokines, including transforming growth factor beta-1 and platelet-derived growth factor. Mild corneal injuries self-repair, but greater injuries lead to corneal haze/scars/fibrosis and vision loss due to disruptions in the ECM, autophagy, and normal wound healing processes. Presently, the precise role of autophagy and ECM remodeling in corneal wound healing is elusive. This review discusses recent trends in autophagy and ECM modulation in the context of corneal wound healing and homeostasis.
Highlights
Autophagy is a self-degradative, robust mechanism for disposing of and recycling defective intracellular structures and substances from the cells
The corneal extracellular matrix (ECM) is regulated by several factors, including autophagy, wound healing process, myofibroblasts, TGF-β, platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), Matrix metalloproteinases (MMPs)/proteases and many other factors and cells, including limbus
Chemokines, growth factors, and vasoactive factors including IL-1β, IL-6, IL-8, TNF-α, IL-13, TGF-β1, VEGF, PDGF, FGF-2, keratinocyte growth factor, histamine, proteases and chemokine (C-C motif) ligand 2 (CCL2)/monocyte chemoattractant protein 1 (MCP1) that are released from activated mast cells play an important role in many phases of the wound healing process, angiogenesis, collagen production and ECM modulation, and tissue repair [93,94]
Summary
Autophagy is a self-degradative, robust mechanism for disposing of and recycling defective intracellular structures and substances from the cells It is implicated in cytoprotection, tissue development, tissue plasticity, response to infections, diseases, injuries, regulation of the immune system, and maintaining cellular and tissue-specific microenvironments and functions [1,2,3,4,5]. The corneal wound healing process is highly complex, involving multiple cell types, cytokines and growth factors, as well as autophagic mechanisms [9,13,15,16]. The ECM interacts with various cells and regulates cellular and organ functions, survival, migration, differentiation, organ structure, tissue regrowth/regeneration, tissue repair, and scar formation, as well as controlling many biological activities and maintaining a normal tissue-specific microenvironment [17,20]. This review highlights recent trends in autophagy and ECM modulation in corneal wound healing and homeostasis
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