MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1007/s00018-010-0525-1

Медицинская библиотека · Cellular and molecular life sciences : CMLS · 2010

Alpha7 nicotinic receptors as novel therapeutic targets for inflammation-based diseases.

Bencherif Merouane, Lippiello Patrick M, Lucas Rudolf, Marrero Mario B

СтатьяОбзорПеревод в очереди

Аннотация

In recent years the etiopathology of a number of debilitating diseases such as type 2 diabetes, arthritis, atherosclerosis, psoriasis, asthma, cystic fibrosis, sepsis, and ulcerative colitis has increasingly been linked to runaway cytokine-mediated inflammation. Cytokine-based therapeutic agents play a major role in the treatment of these diseases. However, the temporospatial changes in various cytokines are still poorly understood and attempts to date have focused on the inhibition of specific cytokines such as TNF-α. As an alternative approach, a number of preclinical studies have confirmed the therapeutic potential of targeting alpha7 nicotinic acetylcholine receptor-mediated anti-inflammatory effects through modulation of proinflammatory cytokines. This "cholinergic anti-inflammatory pathway" modulates the immune system through cholinergic mechanisms that act on alpha7 receptors expressed on macrophages and immune cells. If the preclinical findings translate into human efficacy this approach could potentially provide new therapies for treating a broad array of intractable diseases and conditions with inflammatory components.

Для цитирования: Bencherif Merouane, Lippiello Patrick M, Lucas Rudolf, Marrero Mario B. Alpha7 nicotinic receptors as novel therapeutic targets for inflammation-based diseases.. Cellular and molecular life sciences : CMLS. 2010. DOI: 10.1007/s00018-010-0525-1.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.