ArticleAmerican journal of physiology. Heart and circulatory physiology2009
N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 4 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
112 citing papers in PubMed, 4 syntheses or guidelines pooled it, 266 citations in OpenAlex.
- Role of galectin-3 as a biomarker in obstructive sleep apnea: a systematic review and meta-analysis.Sleep & breathing = Schlaf & Atmung · 2023Pooled it
- Clinical Implications of Plasma Galectin-3 in Heart Failure With Preserved Ejection Fraction: A Meta-Analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- Prognostic Value of Serum Galectin-3 in Chronic Heart Failure: A Meta-Analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- Circulating Galectin-3 and Atrial Fibrillation Recurrence after Catheter Ablation: A Meta-Analysis.Cardiovascular therapeutics · 2019Pooled it
- Galectin-3 in heart failure with preserved ejection fraction. A RELAX trial substudy (Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure).JACC. Heart failure · 2015Trial
- Plasma galectin 3 and heart failure risk in the Physicians' Health Study.European journal of heart failure · 2014Trial
- Galectin 3 complements BNP in risk stratification in acute heart failure.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2012Trial
- Myocardial fibrosis and viability: the role of imaging and biomarkers in patients with chronic total occlusion on coronary angiography.Biochemia medica · 2026Review
- Article
- Alms1 KO Rat: A New Model of Cardiometabolic Syndrome With Spontaneous Hypertension.Acta physiologica (Oxford, England) · 2026Article
- Macrophage surface protein Mac-2 mediates inflammatory and stromal stress pathways in doxorubicin-induced cardiac injury.Cardio-oncology (London, England) · 2026Article
- Interleukin-6 blockade modulates monocyte recruitment to protect against diastolic dysfunction associated with inflammatory arthritis.Arthritis research & therapy · 2026Article
- Ac-SDKP and eplerenone confer additive cardioprotection against angiotensin II-induced cardiac injury in C57BL/6J mice.Journal of molecular and cellular cardiology plus · 2025Article
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- The role of immune checkpoints PD-1 and CTLA-4 in cardiovascular complications leading to heart failure.Frontiers in immunology · 2025Review
- Understanding Galectin-3's Role in Diastolic Dysfunction: A Contemporary Perspective.Life (Basel, Switzerland) · 2024Review
- Proteomics couples electrical remodelling to inflammation in a murine model of heart failure with sinus node dysfunction.Cardiovascular research · 2024Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts by inhibiting CHOP-mediated NF-κB expression.Frontiers in pharmacology · 2024Article
- Review
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Galectin-3 (Gal-3) is secreted by activated macrophages. In hypertension, Gal-3 is a marker for hypertrophic hearts prone to develop heart failure. Gal-3 infused in pericardial sac leads to cardiac inflammation, remodeling, and dysfunction. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), a naturally occurring tetrapeptide, prevents and reverses inflammation and collagen deposition in the heart in hypertension and heart failure postmyocardial infarction. In the present study, we hypothesize that Ac-SDKP prevents Gal-3-induced cardiac inflammation, remodeling, and dysfunction, and these effects are mediated by the transforming growth factor (TGF)-beta/Smad3 signaling pathway. Adult male rats were divided into four groups and received the following intrapericardial infusion for 4 wk: 1) vehicle (saline, n = 8); 2) Ac-SDKP (800 microg x kg(-1) x day(-1), n = 8); 3) Gal-3 (12 microg/day, n = 7); and 4) Ac-SDKP + Gal-3 (n = 7). Left ventricular ejection fraction, cardiac output, and transmitral velocity were measured by echocardiography; inflammatory cell infiltration, cardiomyocyte hypertrophy, and collagen deposition in the heart by histological and immunohistochemical staining; and TGF-beta expression and Smad3 phosphorylation by Western blot. We found that, in the left ventricle, Gal-3 1) enhanced macrophage and mast cell infiltration, increased cardiac interstitial and perivascular fibrosis, and causes cardiac hypertrophy; 2) increased TGF-beta expression and Smad3 phosphorylation; and 3) decreased negative change in pressure over time response to isoproterenol challenge, ratio of early left ventricular filling phase to atrial contraction phase, and left ventricular ejection fraction. Ac-SDKP partially or completely prevented these effects. We conclude that Ac-SDKP prevents Gal-3-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction, possibly via inhibition of the TGF-beta/Smad3 signaling pathway.
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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.