ArticleBiomedicines2020
BAY 41-2272 Attenuates CTGF Expression via sGC/cGMP-Independent Pathway in TGFβ1-Activated Hepatic Stellate Cells.
Article in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Cardioprotective Effects of Soluble Guanylate Cyclase and Its α1 Subunit on Myocardial Ischemia/Reperfusion Injury via the PGC-1α/UCP2 Pathway.Journal of cardiovascular pharmacology · 2026Article
- Activation of the Wnt signaling pathway and its role in epithelial-mesenchymal transition and hepatic fibrosis in alveolar echinococcosis.Frontiers in cellular and infection microbiology · 2025Article
- Can Nutraceuticals Support the Treatment of MASLD/MASH, and thus Affect the Process of Liver Fibrosis?International journal of molecular sciences · 2024Review
- Article
- Sarcoma protein kinase inhibition alleviates liver fibrosis by promoting hepatic stellate cells ferroptosis.Open life sciences · 2023Article
- The Soluble Guanylate Cyclase Stimulator BAY 41-2272 Attenuates Transforming Growth Factor β1-Induced Myofibroblast Differentiation of Human Corneal Keratocytes.International journal of molecular sciences · 2022Article
- Current and Emerging Classes of Pharmacological Agents for the Management of Hypertension.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Review
- Mapping of the sGC Stimulator BAY 41-2272 Binding Site on H-NOX Domain and Its Regulation by the Redox State of the Heme.Frontiers in cell and developmental biology · 2022Article
- Pathogenesis of Liver Fibrosis and Its TCM Therapeutic Perspectives.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Extra- and Intra-Cellular Mechanisms of Hepatic Stellate Cell Activation.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Activation of hepatic stellate cells (HSCs) is a critical pathogenic feature of liver fibrosis and cirrhosis. BAY 41-2272 is a canonical non-nitric oxide (NO)-based soluble guanylyl cyclase (sGC) stimulator that triggers cyclic guanosine monophosphate (cGMP) signaling for attenuation of fibrotic disorders; however, the impact of BAY 41-2272 on HSC activation remains ill-defined. Transforming growth factor (TGF)β and its downstream connective tissue growth factor (CTGF or cellular communication network factor 2, CCN2) are critical fibrogenic cytokines for accelerating HSC activation. Here, we identified that BAY 41-2272 significantly inhibited the TGFβ1-induced mRNA and protein expression of CTGF in mouse primary HSCs. Indeed, BAY 41-2272 increased the sGC activity and cGMP levels that were potentiated by two NO donors and inhibited by a specific sGC inhibitor, ODQ. Surprisingly, the inhibitory effects of BAY 41-2272 on CTGF expression were independent of the sGC/cGMP pathway in TGFβ1-activated primary HSCs. BAY 41-2272 selectively restricted the TGFβ1-induced phosphorylation of Akt but not canonical Smad2/3 in primary HSCs. Together, we illustrate a unique framework of BAY 41-2272 for inhibiting TGFβ1-induced CTGF upregulation and HSC activation via a noncanonical Akt-dependent but sGC/cGMP-independent pathway.
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Registered trials
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