uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment
Our study reveals that uPAR loss drives fibrotic remodeling of the cardiac perivascular-like microenvironment and exacerbates TGFβ1-mediated effects, highlighting its potential as a therapeutic target for cardiac fibrosis.
Authors
- Yelena Parfyonova
- Yulia Goltseva (ORCID: https://orcid.org/0000-0002-6367-3785)
- Е. И. Ратнер (ORCID: https://orcid.org/0000-0003-0920-4029)
- Andrew P. Mazar (ORCID: https://orcid.org/0009-0000-3681-6704)
- M. A Boldyreva (ORCID: https://orcid.org/0000-0002-8309-0018)
- К. В. Дергилев (ORCID: https://orcid.org/0000-0003-2712-4997)
- Andrey Shiryaev
- Victoria Stepanova
- Irina Beloglazova
- Alexander Andreev
- Zoya Tsokolaeva
Institutions
- National Research University Higher School of Economics (RU)
- Lomonosov Moscow State University (RU)
- V.A. Negovsky Scientific Research Institute of General Reanimatology (RU)
- National Medical Research Center of Cardiology (RU)
- Moscow State University (TJ)
- Io Therapeutics (United States) (US)
- University of Pennsylvania (US)
Publication Details
- Journal
- Stem Cell Research & Therapy
- Published
- 2026-02-13
- DOI
- https://doi.org/10.1186/s13287-026-04923-8
- Primary Topic
- Cardiac Fibrosis and Remodeling
- Type
- article
- Field-Weighted Citation Impact
- 0.00