ReviewJournal of neuroinflammation2024
The contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome.
Review in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- VLDLR: A Multifunctional receptor in diverse pathophysiological processes.Cell communication and signaling : CCS · 2026Review
- Identification and validation of a novel ferroptosis-related gene signature associated with inherited retinal degeneration in Rd10 mice.Scientific reports · 2026Article
- From environmental exposure to retinal pathology: epidemiological and mechanistic insights into multi-metal driven ocular diseases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Neuroimmune Interactions in Neurodegeneration: The Role of Microglia in Alzheimer's and Parkinson's Disease Pathogenesis.Brain sciences · 2026Review
- Environmental enrichment as a mitochondria-targeting systems strategy across neurodegenerative diseases and retinal dystrophies.Frontiers in neuroscience · 2026Review
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- Tacrolimus modulates the PI3K AKT mTOR pathway in retinal epithelial cells under inflammatory stress.Scientific reports · 2025Article
- Effects of exercise on neuroinflammation in age-related neurodegenerative disorders.European journal of medical research · 2025Review
- Magnetic hyperthermia in oncology: Nanomaterials-driven combinatorial strategies for synergistic therapeutic gains.Materials today. Bio · 2025Review
- The role of IGF2BP2 in macrophage-mediated NLRP3 inflammasome activation in the pathogenesis of dry AMD.Biology direct · 2025Article
- Does uveitis increase the risk of age-related wet macular degeneration? A Mendelian randomization study.International journal of ophthalmology · 2025Article
- Evaluation of Gene Expression and the Regulatory Role of microRNAs Related to the Mitogen-Activated Protein Kinase Signaling Pathway in Human Retinal Pigment Epithelial Cells Treated With Lipopolysaccharide A and Tacrolimus.Mediators of inflammation · 2025Article
- Multi-Drug Resistance and Breast Cancer Progression via Toll-Like Receptors (TLRs) Signaling.Cell biochemistry and biophysics · 2024Review
- Molecular hybridization modification improves the stability and immunomodulatory activity of TP5 peptide.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss, characterised by the dysfunction and death of the photoreceptors and retinal pigment epithelium (RPE). Innate immune cell activation and accompanying para-inflammation have been suggested to contribute to the pathogenesis of AMD, although the exact mechanism(s) and signalling pathways remain elusive. Pattern recognition receptors (PRRs) are essential activators of the innate immune system and drivers of para-inflammation. Of these PRRs, the two most prominent are (1) Toll-like receptors (TLR) and (2) NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3)-inflammasome have been found to modulate the progression of AMD. Mutations in TLR2 have been found to be associated with an increased risk of developing AMD. In animal models of AMD, inhibition of TLR and NLRP3 has been shown to reduce RPE cell death, inflammation and angiogenesis signalling, offering potential novel treatments for advanced AMD. Here, we examine the evidence for PRRs, TLRs2/3/4, and NLRP3-inflammasome pathways in macular degeneration pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.