Abstract
Age-related macular degeneration (AMD), a retinal degenerative disease, is the leading cause of central vision loss among the elderly population in developed countries and an increasing global burden. The major risk is aging, compounded by other environmental factors and association with genetic variants for risk of progression. Although the etiology of AMD is not yet clearly understood, several pathogenic pathways have been proposed, including dysfunction of the retinal pigment epithelium, inflammation, and oxidative stress. The identification of AMD susceptibility genes encoding complement factors and the presence of complement and other inflammatory mediators in drusen, the hallmark deposits of AMD, support the concept that local inflammation and immune-mediated processes play a key role in AMD pathogenesis that may be accelerated through systemic immune activation. In this regard, increased levels of circulating C-reactive protein (CRP) have been associated with higher risk of AMD. Besides being a risk marker for AMD, CRP may also play a role in the progression of the disease as it has been identified in drusen, and we have recently found that its monomeric form (mCRP) induces blood retinal barrier disruption in vitro. In this review, we will address recent evidence that links CRP and AMD pathogenesis, which may open new therapeutic opportunities to prevent the progression of AMD.
Highlights
Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the aging population worldwide
In this context, elevated C-reactive protein (CRP) levels are found both in the blood of AMD patients and in the eyes of carriers of a complement factor H (CFH) polymorphism associated to the risk for developing the disease, providing a molecular clue to AMD pathogenesis and to how genetic risk factors may influence its course [21, 32]
We summarize the main findings that support the implication of CRP in the pathogenesis of AMD and its connection with aging
Summary
Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the aging population worldwide. The disease affects up to 1.75 million individuals alone in the United States, and this number could increase up to 3 million by 2020 [1,2,3]. The projected number of people with AMD in 2020 is 196 million (95% CrI 140–261), which increases to 288 million in 2040 [205–399] [4]. AMD is a complex, degenerative, and progressive disease involving multiple genetic and environmental factors, which can result in severe visual loss. The disease-causing molecular mechanisms remain unknown, inflammatory processes have been implicated by the identification of AMD susceptibility genes encoding complement factors [5, 6] and by the presence of complement proteins in drusen, the hallmark deposits associated with
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