期刊
NATURE
卷 587, 期 7835, 页码 555-566出版社
NATURE PORTFOLIO
DOI: 10.1038/s41586-020-2938-9
关键词
-
资金
- Wellcome Trust Senior Research Fellowship in Clinical Science [219542/Z/19/Z]
- Medical Research Council, a Chan Zuckerberg Initiative Seed Network Grant
- British Heart Foundation
- Tenovus Scotland
- National Institutes of Health [T32DK083251, P30DK097948, K08DK110415, R01DK123233]
- Crohn's and Colitis Foundation
- Rainin Foundation
- Helmsley Charitable Trust through the Stenosis Therapy and Anti-Fibrotic Research (STAR) Consortium
- Cleveland Clinic
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K08DK110415] Funding Source: NIH RePORTER
Fibrosis can affect any organ and is responsible for up to 45% of all deaths in the industrialized world. It has long been thought to be relentlessly progressive and irreversible, but both preclinical models and clinical trials in various organ systems have shown that fibrosis is a highly dynamic process. This has clear implications for therapeutic interventions that are designed to capitalize on this inherent plasticity. However, despite substantial progress in our understanding of the pathobiology of fibrosis, a translational gap remains between the identification of putative antifibrotic targets and conversion of this knowledge into effective treatments in humans. Here we discuss the transformative experimental strategies that are being leveraged to dissect the key cellular and molecular mechanisms that regulate fibrosis, and the translational approaches that are enabling the emergence of precision medicine-based therapies for patients with fibrosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据