Abstract
Age-related macular degeneration (AMD) is the most common cause of irreversible visual impairment among people over 50 years of age, accounting for up to 50% of all cases of legal blindness in Western countries. Although the aging represents the main determinant of AMD, it must be considered a multifaceted disease caused by interactions among environmental risk factors and genetic backgrounds. Mounting evidence and/or arguments document the crucial role of inflammation and immune-mediated processes in the pathogenesis of AMD. Proinflammatory effects secondary to chronic inflammation (e.g., alternative complement activation) and heterogeneous types of oxidative stress (e.g., impaired cholesterol homeostasis) can result in degenerative damages at the level of crucial macular structures, that is photoreceptors, retinal pigment epithelium, and Bruch's membrane. In the most recent years, the association of AMD with genes, directly or indirectly, involved in immunoinflammatory pathways is increasingly becoming an essential core for AMD knowledge. Starting from the key basic-research notions detectable at the root of AMD pathogenesis, the present up-to-date paper reviews the best-known and/or the most attractive genetic findings linked to the mechanisms of inflammation of this complex disease.
| Original language | English |
|---|---|
| Article number | 435607 |
| Journal | Mediators of Inflammation |
| Volume | 2013 |
| DOIs | |
| Publication status | Published - 2013 |
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ASJC Scopus subject areas
- Immunology
- Cell Biology
Cite this
Mechanism of inflammation in age-related macular degeneration : An up-to-date on genetic landmarks. / Parmeggiani, Francesco; Sorrentino, Francesco S.; Romano, Mario R.; Costagliola, Ciro; Semeraro, Francesco; Incorvaia, Carlo; D'Angelo, Sergio; Perri, Paolo; De Nadai, Katia; Bonomo Roversi, Elia; Franceschelli, Paola; Sebastiani, Adolfo; Rubini, Michele.
In: Mediators of Inflammation, Vol. 2013, 435607, 2013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mechanism of inflammation in age-related macular degeneration
T2 - An up-to-date on genetic landmarks
AU - Parmeggiani, Francesco
AU - Sorrentino, Francesco S.
AU - Romano, Mario R.
AU - Costagliola, Ciro
AU - Semeraro, Francesco
AU - Incorvaia, Carlo
AU - D'Angelo, Sergio
AU - Perri, Paolo
AU - De Nadai, Katia
AU - Bonomo Roversi, Elia
AU - Franceschelli, Paola
AU - Sebastiani, Adolfo
AU - Rubini, Michele
PY - 2013
Y1 - 2013
N2 - Age-related macular degeneration (AMD) is the most common cause of irreversible visual impairment among people over 50 years of age, accounting for up to 50% of all cases of legal blindness in Western countries. Although the aging represents the main determinant of AMD, it must be considered a multifaceted disease caused by interactions among environmental risk factors and genetic backgrounds. Mounting evidence and/or arguments document the crucial role of inflammation and immune-mediated processes in the pathogenesis of AMD. Proinflammatory effects secondary to chronic inflammation (e.g., alternative complement activation) and heterogeneous types of oxidative stress (e.g., impaired cholesterol homeostasis) can result in degenerative damages at the level of crucial macular structures, that is photoreceptors, retinal pigment epithelium, and Bruch's membrane. In the most recent years, the association of AMD with genes, directly or indirectly, involved in immunoinflammatory pathways is increasingly becoming an essential core for AMD knowledge. Starting from the key basic-research notions detectable at the root of AMD pathogenesis, the present up-to-date paper reviews the best-known and/or the most attractive genetic findings linked to the mechanisms of inflammation of this complex disease.
AB - Age-related macular degeneration (AMD) is the most common cause of irreversible visual impairment among people over 50 years of age, accounting for up to 50% of all cases of legal blindness in Western countries. Although the aging represents the main determinant of AMD, it must be considered a multifaceted disease caused by interactions among environmental risk factors and genetic backgrounds. Mounting evidence and/or arguments document the crucial role of inflammation and immune-mediated processes in the pathogenesis of AMD. Proinflammatory effects secondary to chronic inflammation (e.g., alternative complement activation) and heterogeneous types of oxidative stress (e.g., impaired cholesterol homeostasis) can result in degenerative damages at the level of crucial macular structures, that is photoreceptors, retinal pigment epithelium, and Bruch's membrane. In the most recent years, the association of AMD with genes, directly or indirectly, involved in immunoinflammatory pathways is increasingly becoming an essential core for AMD knowledge. Starting from the key basic-research notions detectable at the root of AMD pathogenesis, the present up-to-date paper reviews the best-known and/or the most attractive genetic findings linked to the mechanisms of inflammation of this complex disease.
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U2 - 10.1155/2013/435607
DO - 10.1155/2013/435607
M3 - Article
VL - 2013
JO - Mediators of Inflammation
JF - Mediators of Inflammation
SN - 0962-9351
M1 - 435607
ER -