Section of Digestive Diseases, Yale University, New Haven, Connecticut, USA.
Nat Med. 2011 May;17(5):552-3. doi: 10.1038/nm0511-552.
Animal experiments using single organs as models of fibrosis spur therapeutic development toward promising targets, but testing of these therapies in human fibrosis yielded disappointing results and limited efficacy. Finding core pathways relevant in different organs that can become fibrotic will uncover molecules that will prove useful as therapeutic targets in many species, including humans. In ‘Bench to Bedside’, Scott Friedman, Wajahat Mehal and John Iredale discuss this new paradigm in fibrosis research and its potential as a new drug development approach. In ‘Bedside to Bench’, Alison Eddy peruses how the protein encoded by , a gene linked to variable risk for chronic kidney disease and hypertension in humans, may have a role in fibrosis and kidney disease. Uncovering the normal function of UMOD and its gene variants will shed light on the pathogenesis of chronic kidney disease and aid in the discovery of new targets for kidney fibrosis and hypertension.
动物实验中使用单一器官作为纤维化模型，促进了针对有希望靶点的治疗方法的发展，但这些治疗方法在人类纤维化中的测试结果令人失望，疗效有限。寻找在不同可能纤维化的器官中相关的核心途径，将揭示出对包括人类在内的许多物种都有用的治疗靶点的分子。在“从实验室到病床”这一部分，Scott Friedman、Wajahat Mehal 和 John Iredale 讨论了纤维化研究中的这一新范式及其作为新药开发方法的潜力。在“从病床到实验室”这一部分，Alison Eddy 探讨了编码 的蛋白质在人类慢性肾病和高血压的可变风险中可能发挥的作用，以及该蛋白质在纤维化和肾脏疾病中的作用。揭示 UMOD 及其基因突变的正常功能将有助于阐明慢性肾病的发病机制，并有助于发现肾脏纤维化和高血压的新靶点。
