Molecular Insights into Corneal Wound Healing and Inflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1829

Special Issue Editor

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Guest Editor
Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA
Interests: neuroimmune crosstalk mediation of corneal inflammation; potential pharmaceutical treatment against corneal fibrosis; immunotherapy strategies to suppress corneal angiogenesis; modulation of corneal transplant immunity; novel cell-based therapies; corneal tissue engineering and regeneration; new insights in refractive surgery

Special Issue Information

Dear Colleagues,

During its evolution, the cornea has developed an exclusive process of wound healing designed to maintain and regenerate the tissue while preserving its transparency. Despite its similarities to other tissues such as skin, the cornea is characterized by a lack of vessels, dense sensory innervation, and a specific population of immune resident cells, making it a specialized tissue that requires a high level of scientific attention. The active crosstalk between sensory nerves and immune cells is essential for maintaining its avascularity, transparency, and immune privilege; however, alterations in the environment caused by trauma, infection, ocular surface diseases, or surgery trigger the cornea to undergo an active healing process, first to maintain the external barrier of the eye and then to restore its transparency and sensory functions. Multiple cellular events involving cell death, proliferation, migration, differentiation, and extracellular matrix remodeling are orchestrated to effectively repair the damaged tissue; however, the final resolution of the wound healing is a much more complex process in which inflammatory mediators are key components that mediate the balance between full restoration of the corneal integrity and functionality, or fibrosis. While a suitable inflammatory reaction is necessary for infection eradication and proper wound healing, exacerbated inflammation is the main trigger of edema, fibrosis, and loss of sensory function. Despite numerous advances in managing corneal wound healing, inflammatory-related complications such as ocular pain, fibrosis, diabetic keratopathies, dry eye, graft failure, viral infections, or dystrophies, among many others, remain the main public health concerns. In this Special Issue, we welcome all types of manuscripts from both basic and clinical research aimed at elucidating new strategies for modulating the inflammatory response while promoting the restoration of the cornea’s intrinsic functions.

Dr. Tomas Blanco
Guest Editor

Manuscript Submission Information

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  • corneal wound healing
  • corneal transplantation
  • sensory nerves
  • neovascularization
  • fibrosis
  • growth factors
  • cytokines
  • neuropeptides

Published Papers (1 paper)

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16 pages, 6456 KiB  
Effects of Diabetes Mellitus on Corneal Immune Cell Activation and the Development of Keratopathy
by Pier Luigi Surico, Akitomo Narimatsu, Katayoon Forouzanfar, Rohan Bir Singh, Sara Shoushtari, Reza Dana and Tomas Blanco
Cells 2024, 13(6), 532; - 18 Mar 2024
Viewed by 1487
Diabetes mellitus (DM) is one of the most prevalent diseases globally, and its prevalence is rapidly increasing. Most patients with a long-term history of DM present with some degree of keratopathy (DK). Despite its high incidence, the underlying inflammatory mechanism of DK has [...] Read more.
Diabetes mellitus (DM) is one of the most prevalent diseases globally, and its prevalence is rapidly increasing. Most patients with a long-term history of DM present with some degree of keratopathy (DK). Despite its high incidence, the underlying inflammatory mechanism of DK has not been elucidated yet. For further insights into the underlying immunopathologic processes, we utilized streptozotocin-induced mice to model type 1 DM (T1D) and B6.Cg-Lepob/J mice to model type 2 DM (T2D). We evaluated the animals for the development of clinical manifestations of DK. Four weeks post-induction, the total frequencies of corneal CD45+CD11b+Ly-6G myeloid cells, with enhanced gene and protein expression levels for the proinflammatory cytokines TNF-α and IL-1β, were higher in both T1D and T2D animals. Additionally, the frequencies of myeloid cells/mm2 in the sub-basal neural plexus (SBNP) were significantly higher in T1D and T2D compared to non-diabetic mice. DK clinical manifestations were observed four weeks post-induction, including significantly lower tear production, corneal sensitivity, and epitheliopathy. Nerve density in the SBNP and intraepithelial terminal endings per 40x field were lower in both models compared to the normal controls. The findings of this study indicate that DM alters the immune quiescent state of the cornea during disease onset, which may be associated with the progressive development of the clinical manifestations of DK. Full article
(This article belongs to the Special Issue Molecular Insights into Corneal Wound Healing and Inflammation)
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