Abstract

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.

Keywords

FibrosisTranslational researchTransformative learningMedicineClinical trialIdentification (biology)BioinformaticsComputational biologyProfiling (computer programming)Translational medicineNeuroscienceBiologyComputer sciencePathologyPsychology

MeSH Terms

CytokinesFibroblastsFibrosisGastrointestinal MicrobiomeGenomeHumanHumansIntegrinsMacrophagesMesodermPrecision MedicineSingle-Cell AnalysisTransforming Growth Factor betaTranslational ResearchBiomedical

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Publication Info

Year
2020
Type
review
Volume
587
Issue
7835
Pages
555-566
Citations
1542
Access
Closed

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Cite This

Neil C. Henderson, Florian Rieder, Thomas A. Wynn (2020). Fibrosis: from mechanisms to medicines. Nature , 587 (7835) , 555-566. https://doi.org/10.1038/s41586-020-2938-9

Identifiers

DOI
10.1038/s41586-020-2938-9
PMID
33239795
PMCID
PMC8034822

Data Quality

Data completeness: 86%