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特发性肺纤维化中的 A2B 腺苷受体:寻找合适的干预点以阻止疾病进展。

A2B Adenosine Receptor in Idiopathic Pulmonary Fibrosis: Pursuing Proper Pit Stop to Interfere with Disease Progression.

机构信息

Department of Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Airlangga (UNAIR), Surabaya 60132, Indonesia.

Department of Pulmonology and Respiratory Medicine, Universitas Airlangga Teaching Hospital, Surabaya 60015, Indonesia.

出版信息

Int J Mol Sci. 2023 Feb 23;24(5):4428. doi: 10.3390/ijms24054428.

Abstract

Purine nucleotides and nucleosides are involved in various human physiological and pathological mechanisms. The pathological deregulation of purinergic signaling contributes to various chronic respiratory diseases. Among the adenosine receptors, A2B has the lowest affinity such that it was long considered to have little pathophysiological significance. Many studies suggest that A2BAR plays protective roles during the early stage of acute inflammation. However, increased adenosine levels during chronic epithelial injury and inflammation might activate A2BAR, resulting in cellular effects relevant to the progression of pulmonary fibrosis.

摘要

嘌呤核苷酸和核苷参与各种人体生理和病理机制。嘌呤能信号的病理失调导致各种慢性呼吸道疾病。在腺苷受体中,A2B 具有最低的亲和力,因此长期以来被认为具有很小的病理生理意义。许多研究表明,A2BAR 在急性炎症的早期阶段发挥保护作用。然而,在慢性上皮损伤和炎症期间,腺苷水平的升高可能会激活 A2BAR,导致与肺纤维化进展相关的细胞效应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a02/10002355/7a0d46e71d2b/ijms-24-04428-g001.jpg

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