ArticleBMC cardiovascular disorders2025
Baricitinib represses the myocardial fibrosis via blocking JAK/STAT and TGF-β1 pathways in vivo and in vitro.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The JAK1/2 Inhibitor Baricitinib Ameliorates Neuroinflammation and Symptoms in an Animal Model of Essential Tremor.Pharmacology research & perspectives · 2026Article
- The Immune System as a Proarrhythmic Mediator: A Novel Paradigm for the Development of New Antiarrhythmic Therapy.The Canadian journal of cardiology · 2026Review
- USP18 mediates high glucose-induced cardiomyocyte injury by regulating the JAK/STAT signaling pathway through stabilizing FOXC2 expression.Journal of diabetes investigation · 2026Article
- Molecular Mechanisms and Therapeutic Strategies in Heart Failure Due to Dystrophin Deficiency: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- Myocardial fibrosis, the silent instigator of diastolic dysfunction in patients with rheumatoid arthritis.Physiological research · 2025Review
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Abstract
backgroundJAK/STAT pathway is closely involved in the organ fibrotic process. The current study aimed to investigate the impact of baricitinib, an oral selective JAK1/JAK2 inhibitor, on the myocardial fibrosis in vivo and the activation of cardiac fibroblasts in vitro.
methodsThe mouse myocardial fibrosis model was established by isoproterenol (ISO) treatment, then was treated by baricitinib. The activation of mouse cardiac fibroblasts was established by TGF-β1 stimulation, then was treated by baricitinib with several concentrations. Besides, JAK2 was knocked down by small interfering RNA (siRNA) in TGF-β1-stimulated mouse cardiac fibroblasts.
resultsBaricitinib not only attenuated myocardial cell widening, inflammatory infiltration, fibrous tissue, and heart index, but also reduced collagen volume fraction, the expressions of Col1, Col3, α-SMA, Fn, MMP9, and TIMP1 in ISO-induced myocardial fibrosis mice. Meanwhile, baricitinib decreased the expressions of p-STAT3 and TGF-βRII in these mice. Interestingly, in TGF-β1-stimulated cardiac fibroblasts, baricitinib decreased the expressions of Col1, Col3, α-SMA, Fn, MMP9, and TIMP1 in a dose-dependent manner (From 10 to 2000 nM), also exhibited a dose-dependent impact on the expressions of p-STAT3 and TGF-βRII. Finally, JAK2 knockdown by siRNA downregulated the expressions of Col1, Col3, α-SMA, and Fn in TGF-β1-stimulated cardiac fibroblasts.
conclusionInhibition of JAK/STAT pathway by baricitinib represses the myocardial fibrosis in vivo and in vitro, indicating baricitinib may be a treatment option for myocardial fibrosis, while further validation is needed.
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