ArticleCardiovascular research2016
Carfilzomib reverses pulmonary arterial hypertension.
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- Drugs and toxins associated with pulmonary arterial hypertension: from established culprits to novel threats.ERJ open research · 2025Review
- Cancer Drug Bortezomib, a Proteasomal Inhibitor, Triggers Cytotoxicity in Microvascular Endothelial Cells via Multi-Organelle Stress.bioRxiv : the preprint server for biology · 2025Article
- Review
- Canagliflozin differentially modulates carfilzomib-induced endoplasmic reticulum stress in multiple myeloma and endothelial cells.Archives of toxicology · 2025Article
- Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells.The Kaohsiung journal of medical sciences · 2024Article
- Cancer Therapy-Associated Pulmonary Hypertension and Right Ventricular Dysfunction: Etiologies and Prognostic Implications.Reviews in cardiovascular medicine · 2024Review
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
- Exploring the pathogenesis of pulmonary vascular disease.Frontiers in medicine · 2024Review
- Transcriptional profiles of pulmonary artery endothelial cells in pulmonary hypertension.Scientific reports · 2023Article
- Cancer Therapy-Related Pulmonary Hypertension: A Review of Mechanisms and Implications for Clinical Practice.Anatolian journal of cardiology · 2023Review
- P53: Stability from the Ubiquitin-Proteasome System and Specific 26S Proteasome Inhibitors.ACS omega · 2022Review
- Oxygen sensing, mitochondrial biology and experimental therapeutics for pulmonary hypertension and cancer.Free radical biology & medicine · 2021Article
- Drug and Solute Transporters in Mediating Resistance to Novel Therapeutics in Multiple Myeloma.ACS pharmacology & translational science · 2021Review
- COVID-19 patients may become predisposed to pulmonary arterial hypertension.Medical hypotheses · 2021Article
- Bortezomib Inhibits Hypoxia-Induced Proliferation by Suppressing Caveolin-1/SOCE/[CaBioMed research international · 2021Article
- Carfilzomib-induced pulmonary hypertension with associated right ventricular dysfunction: A case report.SAGE open medical case reports · 2021Article
- Exploration of the Shared Gene Signatures and Molecular Mechanisms Between Systemic Lupus Erythematosus and Pulmonary Arterial Hypertension: Evidence From Transcriptome Data.Frontiers in immunology · 2021Article
- Myocardial proteomic profile in pulmonary arterial hypertension.Scientific reports · 2020Article
- Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
aimsPulmonary arterial hypertension (PAH) remains a lethal disease with pronounced narrowing of pulmonary vessels due to abnormal cell growth. Agents that can reduce the pulmonary vascular thickness thus have therapeutic potential. The present study investigated the efficacy of carfilzomib (CFZ), a proteasome inhibitor and a cancer chemotherapeutic drug, on reversing PAH. METHODS AND
resultsIn two rat models of PAH, SU5416/hypoxia and SU5416/ovalbumin, CFZ effectively reversed pulmonary vascular remodelling with the promotion of apoptosis and autophagy. In human pulmonary artery smooth muscle cells, knocking down mediators of autophagy attenuated CFZ-induced cell death. The cell death role of autophagy was promoted by the participation of tumour protein p53-inducible nuclear protein 1. CFZ increased the protein ubiquitination, and siRNA knockdown of ubiquitin inhibited cell death, suggesting that CFZ-induced cell death is ubiquitin-dependent. Mass spectrometry demonstrated the ubiquitination of major vault protein and heat shock protein 90 in response to CFZ. The siRNA knockdown of these proteins enhanced CFZ-induced cell death, revealing that they are cell survival factors. CFZ reduced right-ventricular pressure and enhanced the efficacy of a vasodilator, sodium nitroprusside. While no indications of CFZ toxicity were observed in the right ventricle of PAH rats, apoptosis was promoted in the left ventricle. Apoptosis was prevented by dexrazoxane or by pifithrin-α without interfering with the efficacy of CFZ to reverse pulmonary vascular remodelling.
conclusionThe addition of anti-tumour agents such as CFZ along with cardioprotectants to currently available vasodilators may be a promising way to improve PAH therapy.
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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.