Editorial – Connective Tissue Growth Factor: A Key Factor Among Mediators of Tissue Fibrosis

Sheibani, Nader

doi:10.18502/jovr.v17i4.12294

Cited by 2 publications

(2 citation statements)

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“…Furthermore, TSP1 has been shown to interact with various signaling pathways that are implicated in AMD. For instance, TSP1 can activate transforming growth factor-beta (TGF-β), a signaling molecule associated with fibrosis and scarring in the late stages of AMD [ 86 , 100 , 101 , 102 , 103 ]. TSP1 can also interact with the CD36 receptor, which is involved in the clearance of drusen, deposits that accumulate in the retina of patients with AMD [ 104 , 105 ].…”

Section: Thrombospondin-1 (Tsp1) and Pathogenesis Of Amdmentioning

confidence: 99%

Choroidal Mast Cells and Pathophysiology of Age-Related Macular Degeneration

Malih,

Song,

Sorenson

et al. 2023

Cells

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Age-related macular degeneration (AMD) remains a leading cause of vision loss in elderly patients. Its etiology and progression are, however, deeply intertwined with various cellular and molecular interactions within the retina and choroid. Among the key cellular players least studied are choroidal mast cells, with important roles in immune and allergic responses. Here, we will review what is known regarding the pathophysiology of AMD and expand on the recently proposed intricate roles of choroidal mast cells and their activation in outer retinal degeneration and AMD pathogenesis. We will focus on choroidal mast cell activation, the release of their bioactive mediators, and potential impact on ocular oxidative stress, inflammation, and overall retinal and choroidal health. We propose an important role for thrombospondin-1 (TSP1), a major ocular angioinflammatory factor, in regulation of choroidal mast cell homeostasis and activation in AMD pathogenesis. Drawing from limited studies, this review underscores the need for further comprehensive studies aimed at understanding the precise roles changes in TSP1 levels and choroidal mast cell activity play in pathophysiology of AMD. We will also propose potential therapeutic strategies targeting these regulatory pathways, and highlighting the promise they hold for curbing AMD progression through modulation of mast cell activity. In conclusion, the evolving understanding of the role of choroidal mast cells in AMD pathogenesis will not only offer deeper insights into the underlying mechanisms but will also offer opportunities for development of novel preventive strategies.

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Section: Thrombospondin-1 (Tsp1) and Pathogenesis Of Amdmentioning

confidence: 99%

Choroidal Mast Cells and Pathophysiology of Age-Related Macular Degeneration

Malih,

Song,

Sorenson

et al. 2023

Cells

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“…Unfortunately, targeting many of these cells and pathways has proven ineffective in the prevention and reversal of fibrotic responses in various diseases. Numerous growth factors including TGF-β, PDGF, CTGF, VEGF-A, and TNF-α have profibrotic activities and contribute to ocular fibrosis through the activation of their downstream signaling events ( 6 ). However, the unique contribution of these pathways and the target cells involved suggests a multi-step process whose involvement in different steps needs further investigation.…”

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confidence: 99%

Editorial: Ocular fibrosis: molecular and cellular mechanisms and treatment modalities

Sorenson,

Belecky-Adams,

Sheibani

2024

Front. Ophthalmol.

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Editorial on the Research TopicOcular fibrosis: molecular and cellular mechanisms and treatment modalities Tissue fibrosis occurs as an excessive repair response to mechanical damage, inflammation, ischemia, and degeneration, leading to irreversible scar formation (1). The excessive proliferation and deposition of various extracellular matrix (ECM) proteins are mediated through the transition of various cell types to myofibroblast-like cells. These cell types include epithelial cells, fibroblasts, vascular cells, glial cells, and inflammatory cells (2). The noted phenotypic and functional changes are considered major events during the fibrotic process with severe alterations in the tissue integrity and function (3,4). Fibrosis contributes to the severity of pathologies in many chronic inflammatory diseases in the eye including retinopathy of prematurity, proliferative diabetic retinopathy (PDR), age-related macular degeneration (AMD), and glaucoma (1, 5). Although the mechanisms of fibrogenesis have been extensively studied, the exact molecular and cellular events that drive this destructive tissue insult remain unresolved and may vary in a tissue, cell, and context-dependent manner. Despite great advances in our knowledge regarding its etiology, effective treatment of fibrogenesis presents an unmet challenge.Numerous in vitro and in vivo models of fibrogenesis have helped gain insight into the role of various factors and their impact on intracellular mechanisms that drive the changes associated with fibrotic responses. Unfortunately, targeting many of these cells and pathways has proven ineffective in the prevention and reversal of fibrotic responses in Frontiers in Ophthalmology frontiersin.org 01

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Editorial – Connective Tissue Growth Factor: A Key Factor Among Mediators of Tissue Fibrosis

Abstract: This is an Editorial and does not have an abstract. Please download the PDF or view the article HTML.

Cited by 2 publications

References 44 publications

Choroidal Mast Cells and Pathophysiology of Age-Related Macular Degeneration

Choroidal Mast Cells and Pathophysiology of Age-Related Macular Degeneration

Editorial: Ocular fibrosis: molecular and cellular mechanisms and treatment modalities

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