Renin-angiotensin system hyperactivation can induce inflammation and retinal neural dysfunction

Toshihide Kurihara, Yoko Ozawa, Susumu Ishida, Hideyuki Okano, Kazuo Tsubota

研究成果: Review article査読

35 被引用数 (Scopus)

抄録

The renin-angiotensin system (RAS) is a hormone system that has been classically known as a blood pressure regulator but is becoming well recognized as a proinflammatory mediator. In many diverse tissues, RAS pathway elements are also produced intrinsically, making it possible for tissues to respond more dynamically to systemic or local cues. While RAS is important for controlling normal inflammatory responses, hyperactivation of the pathway can cause neural dysfunction by inducing accelerated degradation of some neuronal proteins such as synaptophysin and by activating pathological glial responses. Chronic inflammation and oxidative stress are risk factors for high incidence vision-threatening diseases such as diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma. In fact, increasing evidence suggests that RAS inhibition may actually prevent progression of various ocular diseases including uveitis, DR, AMD, and glaucoma. Therefore, RAS inhibition may be a promising therapeutic approach to fine-tune inflammatory responses and to prevent or treat certain ocular and neurodegenerative diseases.

本文言語English
論文番号581695
ジャーナルInternational Journal of Inflammation
2012
DOI
出版ステータスPublished - 2012

ASJC Scopus subject areas

  • 免疫アレルギー学

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