ArticleScientific reports2024
Semaglutide ameliorates pressure overload-induced cardiac hypertrophy by improving cardiac mitophagy to suppress the activation of NLRP3 inflammasome.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Semaglutide exerts neuroprotective effects by blocking the interleukin-17/NOD-like receptor family pyrin domain containing 3-mediated neuroinflammation pathway after traumatic brain injury.Neural regeneration research · 2026Article
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- GLP-1 Receptor Agonists in Cardiac Surgery: From Metabolic Drug to Potential Perioperative Cardioprotective Agent.Journal of cardiovascular development and disease · 2026Review
- Exploring the therapeutic potential of GLP-1 receptor agonists in pulmonary arterial hypertension.ERJ open research · 2026Review
- Semaglutide restores metabolic and structural homeostasis along the gut-heart-metabolic axis in a cafeteria diet-induced obesity model.Scientific reports · 2026Article
- GLP-1 and the cardiovascular system.The Journal of clinical investigation · 2026Review
- A Comprehensive Review on the Cardioprotective and Nephroprotective Effects of Semaglutide, and Its Therapeutic Efficacy and Mechanisms in Cardiorenal Syndrome.Drug design, development and therapy · 2026Review
- The role of the NLRP3 inflammasome in hypertension-related chronic heart failure and its potential therapeutic targets.Frontiers in immunology · 2026Article
- Renal denervation attenuates cardiac dysfunction in HFpEF by inhibiting the ATP-P2X7-NLRP3 inflammasome axis.Basic research in cardiology · 2025Article
- Therapeutic Modulation of Mitophagy by Cafestol in Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis.Nutrients · 2025Article
- Antiinflammatory actions of glucagon-like peptide-1-based therapies beyond metabolic benefits.The Journal of clinical investigation · 2025 · on this mapReview
- Cardiomyopathy in Older Adults.Current cardiology reports · 2025Review
- Semaglutide and adenosine alleviate obesity-induced kidney injury, with observed modulation of the Txnip/NLRP3 pathway.Diabetology & metabolic syndrome · 2025Article
- Danuglipron Ameliorates Pressure Overload-Induced Cardiac Remodelling Through the AMPK Pathway.Journal of cellular and molecular medicine · 2025Article
- Diminazine protects against cardiac aging through the improvement of mitophagy and apoptosis in aging rats induced by D-galactose.BMC cardiovascular disorders · 2025Article
- Beyond weight loss: the potential of glucagon-like peptide-1 receptor agonists for treating heart failure with preserved ejection fraction.Heart failure reviews · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- The mechanism of secreted frizzled-related protein 1 in alleviating cardiomyocyte injury and heart failure.Frontiers in cardiovascular medicine · 2025Review
- Mechanisms and Prevention Strategies of Macrophage Involvement in the Progression From Hypertension to Heart Failure.International journal of hypertension · 2025Review
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6 authors.
Funding
Abstract
Pathological cardiac hypertrophy is an important cause of heart failure(HF). Recent studies reveal that glucagon-like peptide-1 receptor (GLP1R) agonists can improve mortality and left ventricular ejection fraction in the patients with type 2 diabetes and HF. The present study aims to investigate whether semaglutide, a long-acting GLP1R agonist, can ameliorate cardiac hypertrophy induced by pressure overload, and explore the potential mechanism. The rats were performed transverse aortic constriction (TAC) to mimic pressure overload model. The rats were divided into four groups including Sham, TAC, TAC + semaglutide, and TAC + semaglutide + HCQ (hydroxychloroquine, an inhibitor of mitophagy). The rats in each experimental group received their respective interventions for 4 weeks. The parameters of left ventricular hypertrophy(LVH) were measured by echocardiography, Hematoxylin-eosin (HE) staining, western-blot and immunohistochemistry (IHC), respectively. The changes of mitophagy were reflected by detecting cytochrome c oxidase subunit II (COXII), LC3II/LC3I, mitochondria, and autophagosomes. Meanwhile, NLRP3, Caspase-1, and interleukin-18 were detected to evaluate the activation of NLRP3 inflammasome in each group. The results suggest that LVH, impaired mitophagy, and activation of NLRP3 inflammasome were present in TAC rats. Semaglutide significantly reduced LVH, improve mitophagy, and down-regulated NLRP3 inflammatory signal pathway in TAC rats. However, the reversed effect of semaglutide on cardiac hypertrophy was abolished by HCQ, which restored the activation of NLRP3 inflammasome suppressed by improved mitophagy. In conclusion, semaglutide ameliorates the cardiac hypertrophy by improving cardiac mitophagy to suppress the activation of NLRP3 inflammasome. Semaglutide may be a novel potential option for intervention of cardiac hypertrophy induced by pressure overload.
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