ArticleAmerican journal of translational research2018
FGF21 protects myocardial ischemia-reperfusion injury through reduction of miR-145-mediated autophagy.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
44 citing papers in PubMed, 80 citations in OpenAlex.
- Mitokines as bioenergetic stress signals in cardiovascular disease: mitochondrial communication, endocrine adaptation, and translational implications.Journal of bioenergetics and biomembranes · 2026Review
- FGF21-FGFR1 signaling protects against cardiac hypertrophy by regulating PINK1-mediated mitophagy pathway.Journal of advanced research · 2026Article
- LncRNAiScience · 2026Article
- Functions of FGF21 and its role in cardiac hypertrophy.Journal of advanced research · 2026Review
- Silent controllers: non-coding RNAs drive autophagic response in myocardial ischemia reperfusion injury.Frontiers in cardiovascular medicine · 2026Review
- FGF21 Blunts Cardiac Ischemia/Reperfusion Injury by Promoting Autophagic Flux Via Stat1/Irgm1 Pathway.Journal of cardiovascular translational research · 2025Article
- miR-145b/AP2B1 Axis Contributes to Noise-induced Sensorineural Hearing Loss In a Male Mouse Model.Cell biochemistry and biophysics · 2025Article
- NNMT/1-MNA protects against hepatic ischemia-reperfusion injury through the AKT/FOXO1/ANGPT2/JNK axis.Nature communications · 2025Article
- Evidence and perspectives on miRNA, circRNA, and lncRNA in myocardial ischemia-reperfusion injury: a bibliometric study.Journal of cardiothoracic surgery · 2025Article
- Inhibition of Taurine-upregulated Gene 1 Upregulates MiR-34a-5p to Protect against Myocardial Ischemia/ReperfusionCombinatorial chemistry & high throughput screening · 2025Article
- Melatonin Reduces Mito-Inflammation in Ischaemic Hippocampal HT22 Cells and Modulates the cGAS-STING Cytosolic DNA Sensing Pathway and FGF21 Release.Journal of cellular and molecular medicine · 2024Article
- FGFR4 Is Required for Concentric Growth of Cardiac Myocytes during Physiologic Cardiac Hypertrophy.Journal of cardiovascular development and disease · 2024Article
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Fibroblast Growth Factor 21 Suppressed Neutrophil Extracellular Traps Induced by Myocardial Ischemia/Reperfusion Injury via Adenosine Monophosphate-Activated Protein Kinase.Cardiology research · 2024Article
- Brown adipose tissue-derived FGF21 mediates the cardioprotection of dexmedetomidine in myocardial ischemia/reperfusion injury.Scientific reports · 2024Article
- Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress.Experimental and therapeutic medicine · 2024Article
- Bidirectional negative feedback actions of DNMT3A and miR-145 in regulating autophagy in cardiac fibroblasts and affecting myocardial fibrosis.Journal of bioenergetics and biomembranes · 2023Article
- Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023Review
- Article
- Mechanism of fibroblast growth factor 21 in cardiac remodeling.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsFibroblast growth factor 21 (FGF21) plays a critical role in protecting against myocardial ischemia/reperfusion (I/R) injury. However, the molecular mechanism is not completely understood. Here, we aimed to examine whether miRNA-145 (miR-145) is involved in FGF21 protection against myocardial I/R injury through angiopoietin-2 (Angpt2) and autophagy.
methodsWe established a rat myocardial I/R model and H9c2 hypoxia/reoxygenation (H/R) model. After administration of FGF21 in the rat I/R model, the infarct size, morphological changes and apoptosis in myocardium were determined by 2,3,5-triphenyltetrazolium chloride (TTC), hematoxylin and eosin (HE), and Masson's trichrome staining, and TUNEL assay, respectively. The expression levels of miR-145 and Angpt2 were evaluated by quantitative real-time PCR (qRT-PCR), Western blotting and immunohistochemical (IHC) staining. The activity of lactate dehydrogenase (LDH), TNF-α and IL-6 were assayed. Using a dual-luciferase reporter system, the targeted role of miR-145 on Angpt2 was studied. After transfection with miR-145 inhibitor, H9c2 cells were subjected to stimulated H/R with or without FGF21 treatment. The expression of Angpt2 was assessed while cell apoptosis and cell migration assays were performed.
resultsFGF21 significantly decreased infarction after I/R, ameliorated I/R-induced cell apoptosis, and inhibited I/R-induced LDH, TNF-α and IL-6 in serum. FGF21 inhibited I/R-induced decrease in miR-145 level, increase in Angpt2 expression and decrease in autophagy; FGF21 also upregulated LC3-B and Beclin1 levels. miR-145 directly targeted Angpt2. The roles of FGF21 in expression of miR-145 and Angpt2 and activation of autophagy after H/R were reversed by miR-145 inhibitor. In addition, the FGF21-inhibited cell apoptosis and FGF21-promoted migration after H/R were restored by miR-145 inhibitor.
conclusionFGF21 protects myocardial cells against I/R injury by promoting an increase in miR-145 levels and autophagy while inhibiting Angpt2 expression, suggesting a novel therapeutic strategy for protecting against myocardial I/R injury.
Indexed as
Identifiers
30662618PMC6291727W2989678406What 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.