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Complement C3-Targeted Therapy: Replacing Long-Held Assertions with Evidence-Based Discovery
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DOI：10.1016/j.it.2017.03.003.png)
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摘要
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Complement dysregulation underlies several inflammatory disorders, and terminal complement inhibition has thus far afforded significant clinical gains. Nonetheless, emerging pathologies, fueled by complement imbalance and therapy-skewing genetic variance, underscore the need for more comprehensive, disease-tailored interventions. Modulation at the level of C3, a multifaceted orchestrator of the complement cascade, opens up prospects for broader therapeutic efficacy by targeting multiple pathogenic pathways modulated by C3-triggered proinflammatory crosstalk. Notably, C3 intervention is emerging as a viable therapeutic strategy for renal disorders with predominantly complement-driven etiology, such as C3 glomerulopathy (C3G). Using C3G as a paradigm, we argue that concerns about the feasibility of long-term C3 intervention need to be placed into perspective and weighed against actual therapeutic outcomes in prospective clinical trials.
Keyword:
DENSE DEPOSIT DISEASE
PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA
C3 GLOMERULOPATHY
FACTOR-H
GENETIC-VARIANTS
INNATE IMMUNITY
ACTIVATION
GLOMERULONEPHRITIS
ECULIZUMAB
INHIBITOR
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