Purpose: Proliferative vitreoretinopathy (PVR) occurs in 5%-10% of rhegmatogenous retinal detachment cases and is the principle cause for failure of retinal reattachment surgery. Although there are a number of surgical adjunctive agents available for preventing the development of PVR, all have limited efficacy. Discovering predictive molecular biomarkers to determine the probability of PVR development after retinal reattachment surgery will allow better patient stratification for more targeted drug evaluations.
Methods: Narrative literature review.
Results: We provide a summary of the inflammatory and fibrogenic factors found in ocular fluid samples during the development of retinal detachment and PVR and discuss their possible use as molecular PVR predictive biomarkers.
Conclusions: Studies monitoring the levels of the above factors have found that few if any have predictive biomarker value, suggesting that widening the phenotype of potential factors and a combinatorial approach are required to determine predictive biomarkers for PVR.
Translational Relevance: The identification of relevant biomarkers relies on an understanding of disease signaling pathways derived from basic science research. We discuss the extent to which those molecules identified as biomarkers and predictors of PVR relate to disease pathogenesis and could function as useful disease predictors. (http://www.umin.ac.jp/ctr/ number, UMIN000005604).
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http://dx.doi.org/10.1167/tvst.9.3.23 | DOI Listing |
Sci Rep
January 2025
Nordic Bioscience, Immunoscience, Herlev Hovedgade 205-207, Herlev, 2730, Denmark.
Understanding how inflammatory cytokines influence profibrogenic wound healing responses in fibroblasts is important for understanding the pathogenesis of fibrosis. TNF-α and IL-13 are key cytokines in Th1 and Th2 immune responses, respectively, while TGF-β1 is the principal pro-fibrotic mediator. We show that 12-day fibroblast culture with TNF-α or IL-13 induces fibrogenesis, marked by progressively increasing type III and VI collagen formation, and that TGF-β1 co-stimulation amplifies these effects.
View Article and Find Full Text PDFLife (Basel)
December 2024
Department of Pharmacology and Toxicology (Biochemistry Subdivision), College of Pharmacy, Taibah University, Madinah 41411, Saudi Arabia.
Being a central organ in homeostasis and maintaining the health of the biological system, kidneys are exposed to variable toxicants. Long-term exposure to nephrotoxic molecules causes chronic renal damage that causes fibrosis and loss of function. Such damage can be initiated by oxidative stress which provokes inflammation.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFJHEP Rep
January 2025
Vrije Universiteit Brussel, Liver Cell Biology research group, Laarbeeklaan 103, 1090 Brussel, Belgium.
Sci Rep
December 2024
Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, 15, 816 Beon-gil, Jinjudaero, Jinju, 52727, Republic of Korea.
Chronic kidney disease is defined as a progressive loss of kidney function associated with impaired recovery after acute kidney injury. Renal ischemia-reperfusion (IR) induces oxidative stress and inflammatory responses leading to severe tissue damage, where incomplete or maladaptive repair accelerates renal fibrosis and aging. To investigate the role of the purinergic P2Y2 receptor (P2Y2R) in these processes, we used P2Y2R knockout (KO) mice subjected to IR.
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