Rhegmatogenous retinal detachment (RRD) is a sight-threatening condition involving retinal detachment and the accumulation of fluid in the subretinal space. Proliferative vitreoretinopathy (PVR) is a pathologic complication that develops after RRD surgery, and approximately 5-10% of RRD cases develop post-operative PVR. Prolonged inflammation in the wound healing process, epithelial-mesenchymal transition (EMT), retinal pigment epithelial (RPE) cell migration and proliferation, and epiretinal, intraretinal, and subretinal fibrosis are typical in the formation of PVR. RPE cells undergo EMT and become fibroblast-like cells that migrate to the retina and vitreous, promoting PVR formation. Fibroblasts transform into myofibroblasts, which promote fibrosis by overproducing the extracellular matrix (ECM). RPE cells, fibroblasts, glial cells, macrophages, T lymphocytes, and increased ECM production form contractile epiretinal membranes. Cytokine release, complement activation, RPE cells, glial cells, and endothelial cells are all involved in retinal immune responses. Normally, wounds heal within 4 to 6 weeks, including hemostasis, inflammation, proliferation, and remodeling phases. Properly initiated inflammation, complement activation, and the function of neutrophils and glial cells heal the wound in the first stage. In a retinal wound, glial cells proliferate and fill the injured area. Gliosis tries to protect the neurons and prevent damage, but it becomes harmful when it causes scarring. If healing is complicated, prolonged inflammation leads to pathological fibrosis. Currently, there is no preventive treatment for the formation of PVR, and it is worth studying in the future.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817287 | PMC |
| http://dx.doi.org/10.3390/ijms26031025 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Itaconate restrains acute proinflammatory activation of microglia MG after traumatic brain injury in mice.
Sci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFTargeting Neuroinflammation in Preterm White Matter Injury: Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes.
Cell Mol Neurobiol
March 2025
Henan Key Laboratory of Child Brain Injury and Henan Pediatric Clinical Research Center, Institute of Neuroscience and Third Affiliated Hospital of Zhengzhou University, Kangfu Qian Street 7, Zhengzhou, 450052, China.
Neuroinflammation is a key factor in the development of preterm white matter injury (PWMI), leading to glial cell dysfunction, arrest of oligodendrocyte maturation, and long-term neurological damage. As a potential therapeutic strategy, mesenchymal stem cells (MSCs) exhibit significant immunomodulatory and regenerative potential. Recent studies suggest that the primary mechanism of MSC action is their paracrine effects, particularly mediated by extracellular vesicles, with MSC-derived exosomes (MSC-Exos) being the key mediators.
View Article and Find Full Text PDFStudy of Brain Cells in Neurodegenerative Diseases: Raman Microspectroscopy and Scanning Ion-Conductance Microscopy.
Sovrem Tekhnologii Med
March 2025
DSc, Professor, Department of Biophysics, Faculty of Biology; Lomonosov Moscow State University, 1 Leninskiye Gory, Moscow, 119991, Russia; Professor, Department of Physical Materials; National University of Science and Technology "MISIS", 4 Leninsky Prospect, Moscow, 119049, Russia.
Unlabelled: was to identify differences in the structure of the neuronal process network as well as the composition and functional state of cells by studying the bodies and processes of rat brain neurons and astrocytes obtained from pluripotent stem cells of healthy donors and patients with hereditary Parkinson's disease by using a complex of modern high-precision methods such as Raman microspectroscopy, surface-enhanced Raman microspectroscopy, and scanning ion-conductance microscopy.
Materials And Methods: By using Raman spectroscopy and scanning ion-conductance microscopy, the researchers studied the morphology and state of molecules in rat brain neurons and astrocytes induced from pluripotent stem cells of healthy donors and patients with hereditary Parkinson's disease.
Results: The researchers established that typical bands of Raman and surface-enhanced Raman spectra of neurons and astrocytes allowed studying the distribution and conformation of a series of biological molecules (proteins, lipids, cytochromes) in healthy and unhealthy states.
Granular cytoplasmic inclusions in astrocytes and microglial activation in the fetal brain of pigtail macaques in response to maternal viral infection.
Acta Neuropathol Commun
March 2025
Department of Obstetrics and Gynecology, University of Washington, Seattle, WA, USA.
The fetal origins of neuropsychiatric disorders are poorly understood but have been linked to viral or inflammatory injury of the developing brain. The fetal white matter is particularly susceptible to injury as myelination, axonal growth, and deep white matter tracts become established. We have used the pigtail macaque (Macaca nemestrina) to study the maternal and fetal effects of influenza A virus (FLUAV) and Zika virus (ZIKV) infection during pregnancy, in cohorts with different time intervals between inoculation and delivery.
View Article and Find Full Text PDFMesenchymal stem cell-derived extracellular vesicles alleviate autism by regulating microglial glucose metabolism reprogramming and neuroinflammation through PD-1/PD-L1 interaction.
J Nanobiotechnology
March 2025
Department of Children's and Adolescent Health, Public Health College, Harbin Medical University, Harbin, 150081, China.
Neuroinflammation triggered by microglia activation is hallmark of autism spectrum disorder (ASD), and this process includes crucial metabolic reprogramming from oxidative phosphorylation to glycolysis, which may cause neuron loss and functional impairment. The inhibitory immune checkpoint programmed cell death protein 1 (PD-1) on immune cells is an important target for tumor immunotherapy. However, the immunomodulatory effects of PD-1 in ASD remains to be elusive.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!