ArticleHypertension (Dallas, Tex. : 1979)2013
Pulmonary hypertension secondary to left-heart failure involves peroxynitrite-induced downregulation of PTEN in the lung.
Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Getting to the Heart of the Matter: Exploring the Intersection of Cardiovascular Disease, Sex and Race and How Exercise, and Gut Microbiota Influence these Relationships.Reviews in cardiovascular medicine · 2025Review
- Oxidative Stress and Antioxidant Therapy in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Review
- Animal models of pulmonary hypertension due to left heart disease.Animal models and experimental medicine · 2022Review
- Understanding the Pathobiology of Pulmonary Hypertension Due to Left Heart Disease.Circulation research · 2022Review
- PTEN: An Emerging Potential Target for Therapeutic Intervention in Respiratory Diseases.Oxidative medicine and cellular longevity · 2022Review
- PTEN as a Therapeutic Target in Pulmonary Hypertension Secondary to Left-heart Failure: Effect of HO-3867 and Supplemental Oxygenation.Cell biochemistry and biophysics · 2021Review
- Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Protective Effects of Curcumin on Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021Article
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 2020Review
- Synthesis of Spin-Labelled Bergamottin: A Potent CYP3A4 Inhibitor with Antiproliferative Activity.International journal of molecular sciences · 2020Article
- miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways.Molecular medicine reports · 2018Article
- STAT3 activation in infection and infection-associated cancer.Molecular and cellular endocrinology · 2017Review
- HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy.Molecular and cellular biochemistry · 2017Article
- Anticancer potential of diarylidenyl piperidone derivatives, HO-4200 and H-4318, in cisplatin resistant primary ovarian cancer.Cancer biology & therapy · 2016Article
- Targeting constitutively-activated STAT3 in hypoxic ovarian cancer, using a novel STAT3 inhibitor.Oncoscience · 2014Article
- Selective inactivation of PTEN in smooth muscle cells synergizes with hypoxia to induce severe pulmonary hypertension.Journal of the American Heart Association · 2013Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary hypertension (PH) that occurs after left-heart failure (LHF), classified as Group 2 PH, involves progressive pulmonary vascular remodeling induced by smooth muscle cell (SMC) proliferation. However, mechanisms involved in the activation of SMCs remain unknown. The objective of this study was to determine the involvement of peroxynitrite and phosphatase-and-tensin homolog on chromosome 10 (PTEN) in vascular SMC proliferation and remodeling in the LHF-induced PH (LHF-PH). LHF was induced by permanent ligation of left anterior descending coronary artery in rats for 4 weeks. MRI, ultrasound, and hemodynamic measurements were performed to confirm LHF and PH. Histopathology, Western blot, and real-time polymerase chain reaction analyses were used to identify key molecular signatures. Therapeutic intervention was demonstrated using an antiproliferative compound, HO-3867. LHF-PH was confirmed by significant elevation of pulmonary artery pressure (mean pulmonary artery pressure/mm Hg: 35.9±1.8 versus 14.8±2.0, control; P<0.001) and vascular remodeling. HO-3867 treatment decreased mean pulmonary artery pressure to 22.6±0.8 mm Hg (P<0.001). Substantially higher levels of peroxynitrite and significant loss of PTEN expression were observed in the lungs of LHF rats when compared with control. In vitro studies using human pulmonary artery SMCs implicated peroxynitrite-mediated downregulation of PTEN expression as a key mechanism of SMC proliferation. The results further established that HO-3867 attenuated LHF-PH by decreasing oxidative stress and increasing PTEN expression in the lung. In conclusion, peroxynitrite and peroxynitrite-mediated PTEN inactivation seem to be key mediators of lung microvascular remodeling associated with PH secondary to LHF.
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