ArticleInternational journal of molecular sciences2019
Caffeic Acid Phenethyl Ester Rescues Pulmonary Arterial Hypertension through the Inhibition of AKT/ERK-Dependent PDGF/HIF-1α In Vitro and In Vivo.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Bortezomib Suppresses Abnormal Proliferation, Migration, and Phenotypic Switching of Aortic Smooth Muscle Cells.Acta Cardiologica Sinica · 2026Article
- Pulmonary Hypertension Molecular Switch: HIF Signaling Pathway.Pulmonary circulation · 2026Review
- Caffeic acid phenethyl ester induced apoptosis in chronic myeloid leukemia cells by inhibiting mitochondrial complex I.Scientific reports · 2026Article
- Immunomodulatory Role of Propolis in Hypoxia and in the Tumor Microenvironment.Molecules (Basel, Switzerland) · 2025Review
- Caffeic acid phenethyl ester protects renal tubular epithelial cells against ferroptosis in diabetic kidney disease via restoring PINK1-mediated mitophagy.Molecular medicine (Cambridge, Mass.) · 2025Article
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Biomarkers in COPD-Associated PH/CCP: Circulating Molecules and Cell-Intrinsic Marker.International journal of chronic obstructive pulmonary disease · 2025Review
- Caffeic acid phenethyl ester restores mitochondrial homeostasis against peritoneal fibrosis induced by peritoneal dialysis through the AMPK/SIRT1 pathway.Renal failure · 2024Article
- 2023 TSOC-TACVPR-TACPAH Consensus Statement of the Rehabilitation on Patients with Pulmonary Hypertension.Acta Cardiologica Sinica · 2024Article
- Pulmonary Hypertension: Pharmacological and Non-Pharmacological Therapies.Life (Basel, Switzerland) · 2024Review
- PTGES is involved in myofibroblast differentiation via HIF-1α-dependent glycolysis pathway.Journal of cellular and molecular medicine · 2024Article
- Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells.The Kaohsiung journal of medical sciences · 2024Article
- Article
- Application of homocysteine as a non-invasive and effort-free measurements for risk assessment of patients with pulmonary hypertension.Cardiology journal · 2024Article
- Caffeic Acid Phenethyl Ester: A Potential Therapeutic Cancer Agent?Current medicinal chemistry · 2024Review
- Expression and regulation of HIF-1a in hypoxic pulmonary hypertension: Focus on pathological mechanism and Pharmacological Treatment.International journal of medical sciences · 2024Review
- Caffeic Acid Phenethyl Ester (CAPE): Biosynthesis, Derivatives and Formulations with Neuroprotective Activities.Antioxidants (Basel, Switzerland) · 2023Review
- Characterization and evaluation of Colombian propolis on the intestinal integrity of broilers.Poultry science · 2022Article
- Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension.Journal of clinical medicine · 2022Review
- MMP-10 from M1 macrophages promotes pulmonary vascular remodeling and pulmonary arterial hypertension.International journal of biological sciences · 2022Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial proliferation and remodeling, resulting in a specific increase in right ventricle systolic pressure (RVSP) and, ultimately right ventricular failure. Recent studies have demonstrated that caffeic acid phenethyl ester (CAPE) exerts a protective role in NF-κB-mediated inflammatory diseases. However, the effect of CAPE on PAH remains to be elucidated. In this study, monocrotaline (MCT) was used to establish PAH in rats. Two weeks after the induction of PAH by MCT, CAPE was administrated by intraperitoneal injection once a day for two weeks. Pulmonary hemodynamic measurements and pulmonary artery morphological assessments were examined. Our results showed that administration of CAPE significantly suppressed MCT-induced vascular remodeling by decreasing the HIF-1α expression and PDGF-BB production, and improved in vivo RV systolic performance in rats. Furthermore, CAPE inhibits hypoxia- and PDGF-BB-induced HIF-1α expression by decreasing the activation of the AKT/ERK pathway, which results in the inhibition of human pulmonary artery smooth muscle cells (hPASMCs) proliferation and prevention of cells resistant to apoptosis. Overall, our data suggest that HIF-1α is regarded as an alternative target for CAPE in addition to NF-κB, and may represent a promising therapeutic agent for the treatment of PAH diseases.
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