首页> 外文期刊>Trends in pharmacological sciences >Too much of a good thing: adenosine overload in adenosine-deaminase-deficient mice.
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Too much of a good thing: adenosine overload in adenosine-deaminase-deficient mice.

机译:太好了:腺苷脱氨酶缺乏症小鼠的腺苷超负荷。

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摘要

Chronic lung diseases are associated with persistent lung inflammation and damage. The mechanisms that govern the chronic nature of these disorders are not known. Adenosine is a signaling nucleoside that is generated in hypoxic environments such as that found in the inflamed lung, which suggests that it might serve a regulatory role in chronic lung diseases. Support for this hypothesis comes from studies in adenosine-deaminase-deficient mice where lung adenosine levels accumulate in association with increased lung inflammation and damage. Furthermore, lowering adenosine levels or antagonizing adenosine receptors can reverse pulmonary phenotypes in this model, suggesting that chronic adenosine elevations can affect signaling pathways that mediate aspects of chronic lung disease.
机译:慢性肺部疾病与持续性肺部炎症和损害有关。控制这些疾病的慢性性质的机制尚不清楚。腺苷是在低氧环境(例如发炎的肺中发现)中产生的信号核苷,这表明它可能在慢性肺部疾病中起调节作用。对这一假设的支持来自对腺苷脱氨酶缺乏症小鼠的研究,在这些小鼠中,肺腺苷水平的升高与肺部炎症和损伤的增加有关。此外,降低腺苷水平或拮抗腺苷受体可逆转该模型中的肺表型,表明慢性腺苷升高可影响介导慢性肺病方面的信号通路。

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