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This entry refers to a collective group of messenger RNA (mRNA) transcripts that encode proteins involved in the chronic inflammatory processes driving Age-Related Macular Degeneration (AMD). Chronic inflammation, particularly through the alternative complement pathway and the NLRP3 inflammasome, is a hallmark of both the neovascular (wet) and atrophic (dry) forms of the disease (Ambati & Atkinson, 2012, Nature Reviews Immunology). Key transcripts include those for Complement Factor H (CFH), Complement C3, and Complement Factor B, as well as pro-inflammatory cytokines like IL-6 and TNF-alpha (Kauppinen et al., 2016, Progress in Retinal and Eye Research). While many therapies target the resulting proteins, newer modalities such as antisense oligonucleotides (e.g., IONIS-FB-LRx) specifically target the mRNA transcripts themselves to prevent the synthesis of inflammatory mediators (Jaffe et al., 2021, Ophthalmology). Monitoring the expression levels of these transcripts in ocular tissues or systemic circulation serves as a vital biomarker for disease progression and therapeutic efficacy. Consequently, these transcripts represent both a diagnostic signature and a direct therapeutic entry point for gene-silencing technologies in the treatment of AMD.
Inhibition of the complement cascade and reduction of pro-inflammatory cytokine signaling through protein antagonism or antisense-mediated mRNA degradation.
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