ArticleCardiovascular research2008
Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury.
Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 76 citations in OpenAlex.
- Trial
- Sex differences in leptin levels but not in the leptin response to sacubitril/valsartan in patients with heart failure with reduced ejection fraction.Frontiers in cardiovascular medicine · 2026Article
- Myocardial Infarction in Murine Models of Obesity and Related Metabolic Disorders: The Role of Inflammation.International journal of molecular sciences · 2025Review
- Relationship between Myocardial Adaptive Resistance to Ischemia/Reperfusion and Leptin Receptor Expression in Rats with Metabolic Syndrome.Bulletin of experimental biology and medicine · 2025Article
- Targeting the Brain Leptin-Melanocortin Pathway to Treat Heart Failure.Current hypertension reports · 2024Review
- Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin.International journal of molecular sciences · 2024Review
- leptin b and its regeneration enhancer illustrate the regenerative features of zebrafish hearts.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Central Nervous System Actions of Leptin Improve Cardiac Function After Ischemia-Reperfusion: Roles of Sympathetic Innervation and Sex Differences.Journal of the American Heart Association · 2022Article
- Serum level of total histone 3, H3K4me3, and H3K27ac after non-emergent cardiac surgery suggests the persistence of smoldering inflammation at 3 months in an adult population.Clinical epigenetics · 2022Article
- SOCS3 Ablation in Leptin Receptor-Expressing Cells Causes Autonomic and Cardiac Dysfunctions in Middle-Aged Mice despite Improving Energy and Glucose Metabolism.International journal of molecular sciences · 2022Article
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
- Restoration of Cardiac Function After Myocardial Infarction by Long-Term Activation of the CNS Leptin-Melanocortin System.JACC. Basic to translational science · 2021Article
- Targeting the Brain to Protect the Heart.JACC. Basic to translational science · 2021Article
- Cardioprotective properties of leptin in patients with excessive body mass.Irish journal of medical science · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus.Frontiers in cardiovascular medicine · 2020Review
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Article
- Effects of Cardiovascular Risk Factors on Cardiac STAT3.International journal of molecular sciences · 2018Review
- Beneficial effects of leptin treatment in a setting of cardiac dysfunction induced by transverse aortic constriction in mouse.The Journal of physiology · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
aimsLeptin is elevated under conditions of both obesity and heart failure (HF), and activation of leptin receptor (ObR) signalling is known to increase in vivo cardiac contractility and to have anti-hypertrophic effects on the left ventricle (LV). However, it is unknown whether ObR signalling is altered in cardiomyocytes after myocardial infarction (MI) leading to HF, or if a deficiency in ObR signalling leads to worse HF. METHODS AND
resultsIn separate experimental protocols, C57BL/6J and leptin-deficient (ob/ob) mice underwent open-chest surgery to induce permanent left coronary artery ligation (CAL) or had a sham operation. Subgroups of ob/ob mice examined were lean (food-restricted), obese (food-ad libitum), and leptin repleted. Four weeks post-surgery, cardiac structure and function was examined by echocardiography, and the activation of cardiac leptin signalling was characterized through quantitative PCR, western blotting, and DNA-binding activities. CAL produced echocardiographic evidence of HF in C57BL/6J mice, elevated circulating leptin, increased cardiomyocyte leptin and ObR expression, and activated myocardial signal transducer and activator of transcription-3 (STAT3). In leptin-deficient ob/ob mice, whether lean or obese, CAL caused increased hypertrophy and dilation, decreased contractility of the LV, and worsened survival relative to wildtype or leptin-repleted mice after CAL. In ob/ob mice, activation of cardiac STAT3 signalling after CAL is enhanced in the presence of leptin and parallels the induction of the STAT3-responsive genes, tissue-inhibitor of metalloproteinase-1 and heat shock protein-70.
conclusionThese data demonstrate that HF increases ObR signalling in cardiomyocytes and that activation of ObR signalling improves functional outcomes in chronic ischaemic injury leading to HF.
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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.