» Articles » PMID: 38994958

TGF-β-Based Therapies for Treating Ocular Surface Disorders

Overview
Journal Cells
Publisher MDPI
Date 2024 Jul 12
PMID 38994958
Authors
Affiliations
Soon will be listed here.
Abstract

The cornea is continuously exposed to injuries, ranging from minor scratches to deep traumas. An effective healing mechanism is crucial for the cornea to restore its structure and function following major and minor insults. Transforming Growth Factor-Beta (TGF-β), a versatile signaling molecule that coordinates various cell responses, has a central role in corneal wound healing. Upon corneal injury, TGF-β is rapidly released into the extracellular environment, triggering cell migration and proliferation, the differentiation of keratocytes into myofibroblasts, and the initiation of the repair process. TGF-β-mediated processes are essential for wound closure; however, excessive levels of TGF-β can lead to fibrosis and scarring, causing impaired vision. Three primary isoforms of TGF-β exist-TGF-β1, TGF-β2, and TGF-β3. Although TGF-β isoforms share many structural and functional similarities, they present distinct roles in corneal regeneration, which adds an additional layer of complexity to understand the role of TGF-β in corneal wound healing. Further, aberrant TGF-β activity has been linked to various corneal pathologies, such as scarring and Peter's Anomaly. Thus, understanding the molecular and cellular mechanisms by which TGF-β1-3 regulate corneal wound healing will enable the development of potential therapeutic interventions targeting the key molecule in this process. Herein, we summarize the multifaceted roles of TGF-β in corneal wound healing, dissecting its mechanisms of action and interactions with other molecules, and outline its role in corneal pathogenesis.

Citing Articles

Decorin: matrix-based pan-cancer tumor suppressor.

Appunni S, Saxena A, Ramamoorthy V, Zhang Y, Doke M, Nair S Mol Cell Biochem. 2025; .

PMID: 39954173 DOI: 10.1007/s11010-025-05224-z.


Herpes stromal keratitis erodes the establishment of tissue-resident memory T cell pool in HSV-1 infected corneas.

Setia M, Suvas P, Rana M, Chakraborty A, Suvas S Mucosal Immunol. 2024; 18(1):188-204.

PMID: 39581232 PMC: 11891946. DOI: 10.1016/j.mucimm.2024.11.003.


Lumican/Lumikine Promotes Healing of Corneal Epithelium Debridement by Upregulation of EGFR Ligand Expression via Noncanonical Smad-Independent TGFβ/TBRs Signaling.

Kao W, Zhang J, Venkatakrishnan J, Chang S, Yuan Y, Yamanaka O Cells. 2024; 13(19.

PMID: 39404363 PMC: 11475839. DOI: 10.3390/cells13191599.

References
1.
Dituri F, Cossu C, Mancarella S, Giannelli G . The Interactivity between TGFβ and BMP Signaling in Organogenesis, Fibrosis, and Cancer. Cells. 2019; 8(10). PMC: 6829314. DOI: 10.3390/cells8101130. View

2.
David D, Cardoso J, Marques B, Marques R, Silva E, Santos H . Molecular characterization of a familial translocation implicates disruption of HDAC9 and possible position effect on TGFbeta2 in the pathogenesis of Peters' anomaly. Genomics. 2003; 81(5):489-503. DOI: 10.1016/s0888-7543(03)00046-6. View

3.
Bayati F, Mohammadi M, Valadi M, Jamshidi S, Foma A, Sharif-Paghaleh E . The Therapeutic Potential of Regulatory T Cells: Challenges and Opportunities. Front Immunol. 2021; 11:585819. PMC: 7844143. DOI: 10.3389/fimmu.2020.585819. View

4.
Hjelmeland M, Hjelmeland A, Sathornsumetee S, Reese E, Herbstreith M, Laping N . SB-431542, a small molecule transforming growth factor-beta-receptor antagonist, inhibits human glioma cell line proliferation and motility. Mol Cancer Ther. 2004; 3(6):737-45. View

5.
Cua D, Kastelein R . TGF-beta, a 'double agent' in the immune pathology war. Nat Immunol. 2006; 7(6):557-9. DOI: 10.1038/ni0606-557. View