ArticleAmerican journal of physiology. Lung cellular and molecular physiology2021
Hyaluronan/CD44 axis regulates S100A4-mediated mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Bispecific targeting of CHI3L1 and PD-1 as a therapeutic strategy for pulmonary fibrosis.JCI insight · 2026Article
- CAR T cell therapy for fighting IPF: perspectives on a living drug.Frontiers in immunology · 2026Review
- CD44 as a Central Integrator of Inflammation and Fibrosis: From Molecular Signaling to Environmental Modulation.International journal of molecular sciences · 2025Review
- Increased HA/CD44/TGFβ signaling implicates in renal fibrosis of a Col4a5 mutant Alport mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Cyclic mechanical loading of photopolymerized methacrylated hydrogels for probing interdependent effects of strain, stiffness, and substrate composition in pulmonary fibrogenesis.Scientific reports · 2025Article
- Review
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- Tumor suppressors RBL1 and PTEN are epigenetically silenced in IPF mesenchymal progenitor cells by a CD44/Brg1/PRMT5 regulatory complex.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- What Is on the Horizon for Treatments in Idiopathic Pulmonary Fibrosis?Journal of clinical medicine · 2024Review
- CD44 expression in renal tubular epithelial cells in the kidneys of rats with cyclosporine-induced chronic kidney disease.Journal of toxicologic pathology · 2024Article
- The role of macrophage polarization and cellular crosstalk in the pulmonary fibrotic microenvironment: a review.Cell communication and signaling : CCS · 2024Review
- The bronchoalveolar lavage fluidFrontiers in immunology · 2024Article
- Apelin is expressed in intimal smooth muscle cells and promotes their phenotypic transition.Scientific reports · 2023Article
- Hyaluronan in the pathogenesis of acute and post-acute COVID-19 infection.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Blockade of the pentraxin 3/CD44 interaction attenuates lung injury-induced fibrosis.Clinical and translational medicine · 2022Article
- Effect of Qingfei Huaxian Decoction combined with prednisone acetate on serum inflammatory factors and pulmonary function of patients with idiopathic pulmonary fibrosis.American journal of translational research · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Despite modest improvement in patient outcomes from recent advances in pharmacotherapy targeting fibrogenic signaling pathways, idiopathic pulmonary fibrosis (IPF) remains a major unsolved clinical problem. One reason for this is that available antifibrotic agents slow down but do not arrest fibrotic progression. To arrest fibrotic progression, its obligatory drivers need to be identified. We previously discovered that fibrogenic mesenchymal progenitor cells (MPCs) are key drivers of fibrotic progression in IPF, serving as cells of origin for disease-mediating myofibroblasts. IPF MPCs have high levels of nuclear S100A4, which interacts with the proteasome to promote p53 degradation and self-renewal. However, the mechanism underlying S100A4 accumulation in the nucleus of IPF MPCs remains unknown. Here we show that hyaluronan (HA) is present in the fibroblastic focus together with CD44-expressing MPCs and that ligation of CD44 by HA triggers S100A4 nuclear translocation to support IPF MPC self-renewal. The mechanism involves HA-mediated formation of a CD44/S100A4/transportin 1 complex, which promotes S100A4 nuclear import. In a humanized mouse model of pulmonary fibrosis, IPF MPC fibrogenicity was significantly attenuated by
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