ArticleDiabetologia2007
Enhanced activity of the myocardial Na+/H+ exchanger contributes to left ventricular hypertrophy in the Goto-Kakizaki rat model of type 2 diabetes: critical role of Akt.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Cardiovascular and renal outcomes with sodium glucose co-transporter 2 inhibitors in patients with type 2 diabetes mellitus: A system review and network meta-analysis.Frontiers in pharmacology · 2022Pooled it
- Empagliflozin inhibits increased Na influx in atrial cardiomyocytes of patients with HFpEF.Cardiovascular research · 2024Article
- Empagliflozin and Renal Sodium-Hydrogen Exchange in Healthy Subjects.The Journal of clinical endocrinology and metabolism · 2023Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy.Current drug targets · 2023Article
- Alterations of sodium-hydrogen exchanger 1 function in response to SGLT2 inhibitors: what is the evidence?Heart failure reviews · 2022Review
- The Remaining Conundrum of the Role of the NaReviews in cardiovascular medicine · 2022Review
- Luseogliflozin inhibits high glucose-induced TGF-The Journal of international medical research · 2022Article
- Diabetes, Heart Failure and Beyond: Elucidating the Cardioprotective Mechanisms of Sodium Glucose Cotransporter 2 (SGLT2) Inhibitors.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Review
- A SGLT2 Inhibitor Dapagliflozin Alleviates Diabetic Cardiomyopathy by Suppressing High Glucose-Induced Oxidative StressFrontiers in pharmacology · 2021Article
- Empagliflozin reduces the senescence of cardiac stromal cells and improves cardiac function in a murine model of diabetes.Journal of cellular and molecular medicine · 2020 · on this mapArticle
- Extraglycemic Effects of SGLT2 Inhibitors: A Review of the Evidence.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- SGLT2 Inhibitors: A Novel Player in the Treatment and Prevention of Diabetic Cardiomyopathy.Drug design, development and therapy · 2020Review
- SGLT2 Inhibitors Play a Salutary Role in Heart Failure via Modulation of the Mitochondrial Function.Frontiers in cardiovascular medicine · 2019Review
- Of mice and men: models and mechanisms of diabetic cardiomyopathy.Basic research in cardiology · 2018Review
- Voltage dependence of the CaMolecular and cellular biochemistry · 2018Article
- SGLT2 Inhibitors and Cardiovascular Outcomes: Current Perspectives and Future Potentials.Current diabetes reports · 2018Review
- Direct cardiovascular impact of SGLT2 inhibitors: mechanisms and effects.Heart failure reviews · 2018Review
- Class effects of SGLT2 inhibitors in mouse cardiomyocytes and hearts: inhibition of NaDiabetologia · 2018Article
- The Role of Sodium in Diabetic Cardiomyopathy.Frontiers in physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisDiabetes mellitus is a strong risk factor for the development of heart failure, and left ventricular (LV) hypertrophy has been detected in a significant proportion of diabetic patients. Because several studies have suggested that the Na(+)/H(+) exchanger (NHE1) plays a part in the molecular mechanisms involved in cardiac hypertrophy, we investigated its activity and its role in LV myocytes from the Goto-Kakizaki (GK) rat model of type 2 diabetes. MATERIALS AND
methodsFluorometric measurements were used to assess sarcolemmal NHE1 activity in isolated myocytes. NHE1 levels and the possible molecular pathways driving and/or related to NHE1 activity were investigated in relation to the diabetic LV phenotype.
resultsEnhanced NHE1 activity was associated with LV myocyte hypertrophy. This occurred in the absence of any change in NHE1 protein levels; however, activation of several molecular pathways related to NHE1 activity was demonstrated. Thus, phosphorylation of the extracellular signal-regulated protein kinase (Erk), of the protein kinase Akt (also known as protein kinase B) and of the Ca(2+)/calmodulin-dependent kinase II was increased in GK LV myocytes. Intracellular Ca(2+) levels were also increased. Chronic treatment (10-12 weeks) with the NHE1 inhibitor cariporide normalised NHE1 activity, decreased [Formula: see text] levels and reduced LV myocyte hypertrophy. Moreover, among the various activated pathways, cariporide treatment markedly reduced Akt activity only. CONCLUSIONS/
interpretationThese findings indicate that activation of the Akt pathway represents a likely mechanism mediating the hypertrophic effect of increased NHE1 activity in the GK model of type 2 diabetes.
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.