ArticleJournal of cellular physiology2019
Ranolazine prevents pressure overload-induced cardiac hypertrophy and heart failure by restoring aberrant Na
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 60 citations in OpenAlex.
- Ranolazine effectively improves clinical symptoms in patients with slow flow coronary arteries: a randomized, double-blind, placebo-controlled clinical trial.Naunyn-Schmiedeberg's archives of pharmacology · 2025Trial
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Efficacy of sodium channel blockers in treating myotonia is independent of action potential sodium current block.The Journal of physiology · 2026Article
- Ranolazine as a therapeutic agent for diabetic cardiomyopathy: reducing endoplasmic reticulum stress and inflammation in type 2 diabetic rat model.BMC pharmacology & toxicology · 2025Article
- Enhancement of mitochondrial calcium uptake is cardioprotective against maladaptive hypertrophy by retrograde signaling uptuning Akt.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling the pharmacological and therapeutic potential of Ranolazine beyond antianginal drug use: a new insight.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Potential of natural drug modulation of endoplasmic reticulum stress in the treatment of myocardial injury.Journal of pharmaceutical analysis · 2024Review
- Chronic kidney disease activates the HDAC6-inflammatory axis in the heart and contributes to myocardial remodeling in mice: inhibition of HDAC6 alleviates chronic kidney disease-induced myocardial remodeling.Basic research in cardiology · 2024Article
- CaMK II in Cardiovascular Diseases, Especially CaMK II-δ: Friends or Enemies.Drug design, development and therapy · 2024Review
- CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice.Renal failure · 2023Article
- Virtual drug screen reveals context-dependent inhibition of cardiomyocyte hypertrophy.British journal of pharmacology · 2023Article
- Searching for Effective Treatments in HFpEF: Implications for Modeling the Disease in Rodents.Pharmaceuticals (Basel, Switzerland) · 2023Review
- LncRNAs and CircRNAs in Endoplasmic Reticulum Stress: A Promising Target for Cardiovascular Disease?International journal of molecular sciences · 2023Review
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Driving force of deteriorated cellular environment in heart failure: Metabolic remodeling.Clinics (Sao Paulo, Brazil) · 2023Review
- The Remaining Conundrum of the Role of the NaReviews in cardiovascular medicine · 2022Review
- Moricizine prevents atrial fibrillation by late sodium current inhibition in atrial myocytes.Journal of thoracic disease · 2022Article
- Pathophysiology and Treatment of Diabetic Cardiomyopathy and Heart Failure in Patients with Diabetes Mellitus.International journal of molecular sciences · 2022Review
- RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx.Oxidative medicine and cellular longevity · 2022Article
- ER stress and calcium-dependent arrhythmias.Frontiers in physiology · 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
14 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCardiac hypertrophy and heart failure are characterized by increased late sodium current and abnormal Ca METHODS AND
resultsInhibition of late sodium current with the selective inhibitor ranolazine suppressed cardiac hypertrophy and fibrosis and improved heart function assessed by echocardiography, hemodynamics, and histological analysis in mice exposed to chronic pressure overload induced by transverse aortic constriction (TAC). Ca
conclusionsOur study demonstrates that inhibition of late sodium current with ranolazine improves pressure overload-induced cardiac hypertrophy and systolic and diastolic function by restoring Na
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.