ArticleiScience2025
Targeting CDK7/12/13 functional synergism reverses myofibroblast activation and ameliorates lung fibrosis.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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Abstract
Lung fibrosis, characterized by persistent deposition of extracellular matrix to alveolar areas, is a progressive fibrotic disease, which leads to lung function decline and mortality. At the cellular level, myofibroblast activation and proliferation are the central cellular events of lung fibrosis. Here, through a functional genetics screen, we identify cyclin-dependent kinase 13 (CDK13) as a regulator of pro-fibrotic gene expression. Further analyses show that CDK13 cooperates with CDK12 and CDK7 to synergistically induce myofibroblast activation, contractility, and proliferation. Pharmacological inhibition of CDK7/12/13 by a small molecule inhibitor, THZ1, induces myofibroblast reprogramming and reverses myofibroblast activation
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