ArticleFrontiers in cell and developmental biology2022
Immunosuppressants Tacrolimus and Sirolimus revert the cardiac antifibrotic properties of p38-MAPK inhibition in 3D-multicellular human iPSC-heart organoids.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- PRDM16 modulates aspects of cell cycle dynamics and maturation in human iPSC-derived cardiomyocytes.Stem cell reports · 2026Article
- Human cardiac organoids: multidimensional integration and clinical translation potential.Frontiers in pharmacology · 2026Review
- Tacrolimus modulates the PI3K AKT mTOR pathway in retinal epithelial cells under inflammatory stress.Scientific reports · 2025Article
- Aging-associated interleukin-11 drives the molecular mechanism and targeted therapy of idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
- Generation of mature epicardium derived from human-induced pluripotent stem cells via inhibition of mTOR signaling.Nature communications · 2025Article
- Advanced Cardiovascular Toxicity Screening: Integrating Human iPSC-Derived Cardiomyocytes with 2D In Silico Models.Cardiovascular toxicology · 2025Article
- Three-Dimensional iPSC-Based In Vitro Cardiac Models for Biomedical and Pharmaceutical Research Applications.International journal of molecular sciences · 2024Review
- Three-dimensional cardiac models: a pre-clinical testing platform.Biochemical Society transactions · 2024Review
- Generation of 3D-Multicellular Human iPSC-Heart Organoids for the Noninvasive Assessment of Cardiac Fibrosis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Immunosuppressive Agents-Effects on the Cardiovascular System and Selected Metabolic Aspects: A Review.Journal of clinical medicine · 2023Review
- Gene Modulation with CRISPR-based Tools in Human iPSC-Cardiomyocytes.Stem cell reviews and reports · 2023Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac reactive fibrosis is a fibroblast-derived maladaptive process to tissue injury that exacerbates an uncontrolled deposition of large amounts of extracellular matrix (ECM) around cardiomyocytes and vascular cells, being recognized as a pathological entity of morbidity and mortality. Cardiac fibrosis is partially controlled through the sustained activation of TGF-β1 through IL-11 in fibroblasts. Yet, preclinical studies on fibrosis treatment require human physiological approaches due to the multicellular crosstalk between cells and tissues in the heart. Here, we leveraged an iPSC-derived multi-lineage human heart organoid (hHO) platform composed of different cardiac cell types to set the basis of a preclinical model for evaluating drug cardiotoxicity and assessing cardiac fibrosis phenotypes. We found that the inhibition of the p38-MAPK pathway significantly reduces COL1A1 depositions. Yet, concomitant treatment with organ-rejection immunosuppressant drugs Tacrolimus or Sirolimus reverts this effect, opening new questions on the clinical considerations of combined therapies in reducing fibrosis after organ transplantation.
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