ArticleJournal of molecular and cellular cardiology2010
Benfotiamine improves functional recovery of the infarcted heart via activation of pro-survival G6PD/Akt signaling pathway and modulation of neurohormonal response.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Glucose metabolic dysregulation of diabetes and Its role in atrial fibrillation pathogenesis.Frontiers in cardiovascular medicine · 2025Review
- Benfotiamine improves dystrophic pathology and exercise capacity in mdx mice by reducing inflammation and fibrosis.Human molecular genetics · 2024Article
- Synthetic Thioesters of Thiamine: Promising Tools for Slowing Progression of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Thiamine as a peripheral neuro-protective agent in comparison with N-acetyl cysteine in axotomized rats.Iranian journal of basic medical sciences · 2023Article
- Review
- Endothelial glycocalyx is damaged in diabetic cardiomyopathy: angiopoietin 1 restores glycocalyx and improves diastolic function in mice.Diabetologia · 2022Article
- Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?International journal of molecular sciences · 2021Review
- Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.Journal of cachexia, sarcopenia and muscle · 2021Article
- The Controversial Role of Glucose-6-Phosphate Dehydrogenase Deficiency on Cardiovascular Disease: A Narrative Review.Oxidative medicine and cellular longevity · 2021Review
- Review
- Dysregulation of ghrelin in diabetes impairs the vascular reparative response to hindlimb ischemia in a mouse model; clinical relevance to peripheral artery disease.Scientific reports · 2020Article
- Early dysregulation of cardiac-specific microRNA-208a is linked to maladaptive cardiac remodelling in diabetic myocardium.Cardiovascular diabetology · 2019Article
- Glucose-6-phosphate dehydrogenase is critical for suppression of cardiac hypertrophy by HCell death discovery · 2018Article
- Glucose 6 phosphatase dehydrogenase (G6PD) and neurodegenerative disorders: Mapping diagnostic and therapeutic opportunities.Genes & diseases · 2017Review
- Integration of flux measurements to resolve changes in anabolic and catabolic metabolism in cardiac myocytes.The Biochemical journal · 2017Article
- Augmentation of autophagy by atorvastatin via Akt/mTOR pathway in spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- Test-retest repeatability of myocardial blood flow and infarct size using ¹¹C-acetate micro-PET imaging in mice.European journal of nuclear medicine and molecular imaging · 2015Article
- MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network.Cell stress & chaperones · 2015Article
- Migration towards SDF-1 selects angiogenin-expressing bone marrow monocytes endowed with cardiac reparative activity in patients with previous myocardial infarction.Stem cell research & therapy · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Benfotiamine (BFT) is a transketolase activator that directs glucose to the pentose phosphate pathway. The present study investigated whether BFT improves the recovery after myocardial infarction (MI) and explored underlying mechanisms of protection. Non-diabetic and streptozotocin-induced type 1 diabetic mice were supplemented with BFT (70 mg/kg/day in drinking water) for 4 weeks and then subjected to MI or sham operation. Cardiac function was monitored by echocardiography. At two weeks post-MI, intra-ventricular pressure was measured by Millar tip-catheter and hearts were collected for biochemical, immunohistochemical and expressional analyses. No treatment effect was observed in sham-operated mice. Post-MI mortality was higher in diabetic mice and hemodynamic studies confirmed the worsening effect of diabetes on functional recovery. Furthermore, diabetic mice demonstrated increased cardiomyocyte apoptosis, reduced reparative angiogenesis, larger scars, enhanced oxidative stress, and blunted activation of the pro-survival VEGF receptor-2/Akt/Pim-1 signaling pathway. BFT improved post-MI survival, functional recovery and neovascularization and reduced cardiomyocyte apoptosis and neurohormonal activation in diabetic as well as in non-diabetic mice. In addition, BFT stimulated the activity of pentose phosphate pathway enzymes, leading to reduction of oxidative stress, phosphorylation/activation of VEGF receptor-2 and Akt and increased Pim-1, pBad and Bcl-2 levels. These effects were contrasted on silencing glucose-6-phosphate dehydrogenase, the key enzyme in pentose phosphate pathway, or inhibiting Akt. BFT benefits post-MI recovery through stimulation of pro-survival mechanisms and containment of neurohormonal response. These results may have implications for the treatment of myocardial ischemia.
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