ArticleCommunications biology2024
Contrasting effects of intracellular and extracellular human PCSK9 on inflammation, lipid alteration and cell death.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- In-vivo CRISPR/Base-Editing "One-Shot" Therapies Targeting PCSK9.Current atherosclerosis reports · 2026Review
- Targeting PCSK9 in Vascular Smooth Muscle Cells: An Effective Strategy to Suppress Ferroptosis and Attenuate Abdominal Aortic Aneurysm Progression.Cell proliferation · 2026Article
- Article
- Serum HMGB3 and PCSK9 Levels as Predictors of Early Treatment Response in PediatricInternational journal of general medicine · 2026Article
- Bioinformatics Screening and Preliminary Experimental Verification of Integrated Stress Response-Associated MYC and BAG3 in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026Article
- Hypercholesterolemia as a Causal Risk Factor for COPD: Biomarker Discovery and Therapeutic Implications From NHANES Data.International journal of chronic obstructive pulmonary disease · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is one of the major regulators of low-density lipoprotein receptor (LDLR). Information on role and regulation of PCSK9 in lung is very limited. Our study focuses on understanding the role and regulation of PCSK9 in the lung. PCSK9 levels are higher in Bronchoalveolar lavage fluid (BALF) of smokers with or without chronic obstructive pulmonary diseases (COPD) compared to BALF of nonsmokers. PCSK9-stimulated cells induce proinflammatory cytokines and activation of MAPKp38. PCSK9 transcripts are highly expressed in healthy individuals compared to COPD, pulmonary fibrosis or pulmonary systemic sclerosis. Cigarette smoke extract reduce PCSK9 levels in undifferentiated pulmonary bronchial epithelial cells (PBEC) but induce in differentiated PBEC. PCSK9 inhibition affect biological pathways, induces lipid peroxidation, and higher level of apoptosis in response to staurosporine. Our results suggest that higher levels of PCSK9 in BALF acts as an inflammatory marker. Furthermore, extracellular and intracellular PCSK9 play different roles.
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Registered trials
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