ArticleStem cell reports2021
PCSK9 regulates the NODAL signaling pathway and cellular proliferation in hiPSCs.
Article in Stem cell reports, 2021. 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.
- Role of PCSK9 in hallmarks of cancer: From mechanisms to interventions (Review).Oncology letters · 2026Review
- TGF-β: The Molecular Mechanisms of Atherosclerosis - insights into SMAD Pathways and Gene Therapy Prospects.Current medicinal chemistry · 2026Review
- 1q gain bypasses the selective barrier against aneuploidy in RPE differentiation via wild-type co-culture rescue.Nature communications · 2025Article
- Carfilzomib shows therapeutic potential for reduction of liver fibrosis by targeting hepatic stellate cell activation.Scientific reports · 2024Article
- Dyslipidaemia management in pregnant patients: a 2024 update.European heart journal open · 2024Review
- Targeting PCSK9 reduces cancer cell stemness and enhances antitumor immunity in head and neck cancer.iScience · 2023Article
- PCSK9 Inhibition Regulates Infarction-Induced Cardiac Myofibroblast Transdifferentiation via Notch1 Signaling.Cell biochemistry and biophysics · 2023Article
- Expanding Biology of PCSK9: Roles in Atherosclerosis and Beyond.Current atherosclerosis reports · 2022Review
- Multifunctional polyphenol-based silk hydrogel alleviates oxidative stress and enhances endogenous regeneration of osteochondral defects.Materials today. Bio · 2022Article
- Inhibition of PCSK9 enhances the antitumor effect of PD-1 inhibitor in colorectal cancer by promoting the infiltration of CD8Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proprotein convertase subtilisin kexin type 9 (PCSK9) is a key regulator of low-density lipoprotein (LDL) cholesterol metabolism and the target of lipid-lowering drugs. PCSK9 is mainly expressed in hepatocytes. Here, we show that PCSK9 is highly expressed in undifferentiated human induced pluripotent stem cells (hiPSCs). PCSK9 inhibition in hiPSCs with the use of short hairpin RNA (shRNA), CRISPR/cas9-mediated knockout, or endogenous PCSK9 loss-of-function mutation R104C/V114A unveiled its new role as a potential cell cycle regulator through the NODAL signaling pathway. In fact, PCSK9 inhibition leads to a decrease of SMAD2 phosphorylation and hiPSCs proliferation. Conversely, PCSK9 overexpression stimulates hiPSCs proliferation. PCSK9 can interfere with the NODAL pathway by regulating the expression of its endogenous inhibitor DACT2, which is involved in transforming growth factor (TGF) β-R1 lysosomal degradation. Using different PCSK9 constructs, we show that PCSK9 interacts with DACT2 through its Cys-His-rich domain (CHRD) domain. Altogether these data highlight a new role of PCSK9 in cellular proliferation and development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.