ArticleCardiovascular research2019
Protection against pressure overload-induced right heart failure by uncoupling protein 2 silencing.
Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- Effects of Voluntary Running Wheel Activity and Hypertension on the Brain of Female Spontaneously Hypertensive Rats (SHRs).International journal of molecular sciences · 2026Article
- Acyl-CoA thioesterase 1 (ACOT1) overexpression alleviates heart failure by inhibiting oxidative stress and cardiomyocyte apoptosis through the Kelch-like ECH-associated protein1-NF-E2-related factor2 (KEAP1-NRF2) pathway.Experimental animals · 2026Article
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- Identification of serum C4BPA as a potential diagnostic marker of right ventricular remodelling via proteomic analysis.ESC heart failure · 2025Article
- Molecular Mechanisms of Cardiac Adaptation After Device Deployment.Journal of cardiovascular development and disease · 2025Review
- Dysregulation of Mitochondrial in Pulmonary Hypertension-Related Right Ventricular Remodeling: Pathophysiological Features and Targeting Drugs.Reviews in cardiovascular medicine · 2025Review
- Alisol A ameliorates vascular cognitive impairment via AMPK/NAMPT/SIRT1-mediated regulation of cholesterol and autophagy.Theranostics · 2025Article
- Emerging role and the signaling pathways of uncoupling protein 2 in kidney diseases.Renal failure · 2024Review
- Does Cell-Type-Specific Silencing of Monoamine Oxidase B Interfere with the Development of Right Ventricle (RV) Hypertrophy or Right Ventricle Failure in Pulmonary Hypertension?International journal of molecular sciences · 2024Article
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- Clinical and Molecular Implications of Osteopontin in Heart Failure.Current issues in molecular biology · 2022Review
- Role of Uncoupling Protein 2 Gene Polymorphisms on the Risk of Ischemic Stroke in a Sardinian Population.Life (Basel, Switzerland) · 2022Article
- Effects of voluntary exercise on the expression of browning markers in visceral and subcutaneous fat tissue of normotensive and spontaneously hypertensive rats.Pflugers Archiv : European journal of physiology · 2022Article
- Uncoupling Protein 2 as a Pathogenic Determinant and Therapeutic Target in Cardiovascular and Metabolic Diseases.Current neuropharmacology · 2022Article
- Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021Review
- Downregulation of Uncoupling Protein 2(UCP2) Mediated by MicroRNA-762 Confers Cardioprotection and Participates in the Regulation of Dynamic Mitochondrial Homeostasis of Dynamin Related Protein1 (DRP1) After Myocardial Infarction in Mice.Frontiers in cardiovascular medicine · 2021Article
- Lack of Contribution of p66shc to Pressure Overload-Induced Right Heart Hypertrophy.International journal of molecular sciences · 2020Article
- Cardioprotection in right heart failure.British journal of pharmacology · 2020Review
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
- Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe role of uncoupling protein 2 (UCP2) in cardiac adaptation to pressure overload remains unclear. In a classical model of left ventricular pressure overload genetic deletion of UCP2 (UCP2-/-) protected against cardiac hypertrophy and failure. However, in UCP2-/- mice increased proliferation of pulmonary arterial smooth muscle cells induces mild pulmonary hypertension, right ventricular (RV) hypertrophy, and reduced cardiac output. This suggests a different role for UCP2 in RV and left ventricular adaptation to pressure overload. To clarify this situation in more detail UCP2-/- and wild-type mice were exposed to pulmonary arterial banding (PAB). METHODS AND
resultsMice were analysed (haemodynamics, morphometry, and echocardiography) 3 weeks after PAB or sham surgery. Myocytes and non-myocytes were isolated and analysed separately. Cell shortening of myocytes and fura-2 loading of cardiomyocytes were used to characterize their function. Brd assay was performed to study fibroblast proliferation. Isolated mitochondria were analysed to investigate the role of UCP2 for reactive oxygen species (ROS) production. UCP2 mRNA was 2.7-fold stronger expressed in RV myocytes than in left ventricular myocytes and stronger expressed in non-myocytes compared with myocytes. Three weeks after PAB, cardiac output was reduced in wild type but preserved in UCP2-/- mice. UCP2-/- had increased RV wall thickness, but lower RV internal diameters and displayed a significant stronger fibrosis. Cardiac fibroblasts from UCP2-/- had reduced proliferation rates but higher collagen-1 expression. Myocytes isolated from mice after PAB banding showed preserved function that was further improved by UCP2-/-. Mitochondrial ROS production and respiration was similar between UCP2-/- or wild-type hearts.
conclusionDespite a mild pulmonary hypertension in UCP2-/- mice, hearts from these mice are well preserved against additional pressure overload (severe pulmonary hypertension). This-at least in part-depends on different behaviour of non-myocytes (fibroblasts).
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