ArticleCirculation2012
Therapeutic impact of follistatin-like 1 on myocardial ischemic injury in preclinical models.
Article in Circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 178 citations in OpenAlex.
- FSTL-1 as a Novel Cardiokine of Cardiac Angiogenesis: A Systematic Review.Vascular health and risk management · 2025Pooled it
- Pharmacological attenuation of myocardial reperfusion injury in a closed-chest porcine model: a systematic review.Journal of cardiovascular translational research · 2014Pooled it
- Effect of Omega-3 Polyunsaturated Fatty Acids Supplementation on Body Composition and Circulating Levels of Follistatin-Like 1 in Males With Coronary Artery Disease: A Randomized Double-Blind Clinical Trial.American journal of men's health · 2017Trial
- Exerkines in Cardiovascular-Kidney-Metabolic Syndrome: An Integrative Framework for Mechanisms and Therapeutic Implications-A Narrative Review.Reviews in cardiovascular medicine · 2026Review
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Novel Allogeneic Mitochondria and Associated Organelle Complex Treatment Prevents Myocardial Ischemia-Reperfusion Injury Through Anti-Apoptotic Effects.JACC. Asia · 2026Article
- Signalling pathways regulated by FSTL1 in inflammation and potential therapeutic applications (Review).International journal of molecular medicine · 2026Review
- Acute and Chronic Resistance Training Differentially Modulate Myocardial Angiogenesis-Related Gene Expression in Wistar Rats.Cardiology research and practice · 2026Article
- Electroacupuncture pretreatment alleviates myocardial ischemia injury via brown adipose tissue and BMP3b/Smad1/5 pathway in mice.Adipocyte · 2025Article
- Brown remodeling of white adipose tissue protects against abdominal aortic aneurysm via batokine FSTL1.EMBO molecular medicine · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- The Role of Selected Myokines in the Development of Cardiovascular Diseases, and Their Involvement in Developing Heart Failure in Rheumatoid Arthritis Patients.International journal of molecular sciences · 2025Review
- Decoding the Liver-Heart Axis in Cardiometabolic Diseases.Circulation research · 2025Review
- Skeletal Muscle as a Mediator of Interorgan Crosstalk During Exercise: Implications for Aging and Obesity.Circulation research · 2025Review
- Impact of follistatin-like 1 on cardiac repair processes following myocardial infarction.Frontiers in cell and developmental biology · 2025Review
- Neuromodulatory co-expression in cardiac vagal motor neurons of the dorsal motor nucleus of the vagus.iScience · 2024Article
- Brown adipose tissue-derived FGF21 mediates the cardioprotection of dexmedetomidine in myocardial ischemia/reperfusion injury.Scientific reports · 2024Article
- FSTL1 Accelerates Nucleus Pulposus Cell Senescence and Intervertebral Disc Degeneration Through TLR4/NF-κB Pathway.Inflammation · 2024Article
- Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024Review
- Follistatin-like 1 (FSTL1) levels as potential early biomarker of cardiovascular disease in a Mexican population.Heart and vessels · 2024Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAcute coronary syndrome is a leading cause of death in developed countries. Follistatin-like 1 (FSTL1) is a myocyte-derived secreted protein that is upregulated in the heart in response to ischemic insult. Here, we investigated the therapeutic impact of FSTL1 on acute cardiac injury in small and large preclinical animal models of ischemia/reperfusion and dissected its molecular mechanism. METHODS AND
resultsAdministration of human FSTL1 protein significantly attenuated myocardial infarct size in a mouse or pig model of ischemia/reperfusion, which was associated with a reduction of apoptosis and inflammatory responses in the ischemic heart. Administration of FSTL1 enhanced the phosphorylation of AMP-activated protein kinase in the ischemia/reperfusion-injured heart. In cultured cardiac myocytes, FSTL1 suppressed apoptosis in response to hypoxia/reoxygenation and lipopolysaccharide-stimulated expression of proinflammatory genes through its ability to activate AMP-activated protein kinase. Ischemia/reperfusion led to enhancement of bone morphogenetic protein-4 expression and Smad1/5/8 phosphorylation in the heart, and FSTL1 suppressed the increased phosphorylation of Smad1/5/8 in ischemic myocardium. Treating cardiac myocytes with FSTL1 abolished the bone morphogenetic protein-4-stimulated increase in apoptosis, Smad1/5/8 phosphorylation, and proinflammatory gene expression. In cultured macrophages, FSTL1 diminished lipopolysaccharide-stimulated expression of proinflammatory genes via activation of AMP-activated protein kinase and abolished bone morphogenetic protein-4-dependent induction of proinflammatory mediators.
conclusionsOur data indicate that FSTL1 can prevent myocardial ischemia/reperfusion injury by inhibiting apoptosis and inflammatory response through modulation of AMP-activated protein kinase- and bone morphogenetic protein-4-dependent mechanisms, suggesting that FSTL1 could represent a novel therapeutic target for post-myocardial infarction, acute coronary syndrome.
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What OpenQuestion holds
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.