ArticleJournal of cellular and molecular medicine2018
Irisin inhibits high glucose-induced endothelial-to-mesenchymal transition and exerts a dose-dependent bidirectional effect on diabetic cardiomyopathy.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 70 citations in OpenAlex.
- Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Irisin-induced cardiac fibroblast proliferation is dependent on glucose concentration and is inhibited by WZB117.Molecular biology reports · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Atherosclerosis in diabetes mellitus: novel mechanisms and mechanism-based therapeutic approaches.Nature reviews. Cardiology · 2025Review
- From Skeletal Muscle to Myocardium: Molecular Mechanisms of Exercise-Induced Irisin Regulation of Cardiac Fibrosis.International journal of molecular sciences · 2025Review
- Diabetes-Driven Atherosclerosis: Updated Mechanistic Insights and Novel Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Swimming alleviates myocardial fibrosis of type II diabetic rats through activating miR-34a-mediated SIRT1/PGC-1α/FNDC5 signal pathway.PloS one · 2024Article
- Cardioprotective Effects of Exercise: The Role of Irisin and Exosome.Current vascular pharmacology · 2024Review
- FNDC5 genetic polymorphism in patients with peripartum cardiomyopathy.Caspian journal of internal medicine · 2024Article
- Irisin: A Potentially Fresh Insight into the Molecular Mechanisms Underlying Vascular Aging.Aging and disease · 2023Review
- GDF15 affects venous thrombosis by promoting EndMT through smad2/p-smad2 pathway.Thrombosis journal · 2023Article
- Potential clinical biomarkers and perspectives in diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2023Review
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- miR-132-3p and KLF7 as novel regulators of aortic stiffening-associated EndMT in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2023Article
- The Potential Relationship Between Serum Irisin Concentration With Inflammatory Cytokines, Oxidative Stress Biomarkers, Glycemic Indices and Lipid Profiles in Obese Patients With Type 2 Diabetes Mellitus: A Pilot Study.Journal of the ASEAN Federation of Endocrine Societies · 2023Article
- Obesity accelerates endothelial-to-mesenchymal transition in adipose tissues of mice and humans.Frontiers in cardiovascular medicine · 2023Article
- A Cyclopentanone Compound Attenuates the Over-Accumulation of Extracellular Matrix and Fibrosis in Diabetic Nephropathy via Downregulating the TGF-β/p38MAPK Axis.Biomedicines · 2022Article
- LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway.Molecular medicine reports · 2022Article
- Tumor Necrosis Factor Receptor Superfamily Member 21 Induces Endothelial-Mesenchymal Transition in Coronary Artery Endothelium of Type 2 Diabetes Mellitus.Biomedicines · 2022Article
- The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence indicates that irisin provides beneficial effects in diabetes. However, whether irisin influences the development of diabetic cardiomyopathy (DCM) remains unclear. Therefore, we investigated the potential role and mechanism of action of irisin in diabetes-induced myocardial dysfunction in mice. Type 1 diabetes was induced in mice by injecting streptozotocin, and the diabetic mice were administered recombinant r-irisin (low or high dose: 0.5 or 1.5 μg/g body weight/day, I.P.) or PBS for 16 weeks. Irisin treatment did not alter blood glucose levels in the diabetic mice. However, the results of echocardiographical and histopathological assays indicated that low-dose irisin treatment alleviated cardiac fibrosis and left ventricular function in the diabetic mice, whereas high-dose irisin failed to mitigate the ventricular function impairment and increased collagen deposition. The potential mechanism underlying the effect of low-dose irisin involved irisin-mediated inhibition of high glucose-induced endothelial-to-mesenchymal transition (EndMT); conversely, high-dose irisin treatment enhanced high glucose-induced MMP expression by stimulating MAPK (p38 and ERK) signalling and cardiac fibroblast proliferation and migration. Low-dose irisin alleviated DCM development by inhibiting high glucose-induced EndMT. By contrast, high-dose irisin disrupted normal MMP expression and induced cardiac fibroblast proliferation and migration, which results in excess collagen deposition. Thus, irisin can inhibit high glucose-induced EndMT and exert a dose-dependent bidirectional effect on DCM.
Indexed as
Identifiers
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.