ReviewWiener medizinische Wochenschrift (1946)2012
Calcium handling in human heart failure--abnormalities and target for therapy.
Review in Wiener medizinische Wochenschrift (1946), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Cardiac myosin motor deficits are associated with left ventricular dysfunction in human ischemic heart failure.American journal of physiology. Heart and circulatory physiology · 2023Article
- Association of Repetitive Dosing of Levosimendan with Reduction of NYHA Class and NT-proBNP Levels in Decompensated Heart Failure: A Retrospective Cohort Study.Drugs - real world outcomes · 2022Article
- Enhanced store-operated CaBiology open · 2017Article
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- Clinical Potentials of Cardiomyocytes Derived from Patient-Specific Induced Pluripotent Stem Cells.Journal of clinical medicine · 2014Review
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Safety and Efficacy of Ranolazine for the Treatment of Chronic Angina Pectoris.Clinical medicine insights. Therapeutics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fast cycling of calcium between internal stores and the myofilaments with rapid diffusion down steep concentration gradients provides the cellular basis for cardiac contraction and relaxation. In heart failure, the intracellular Ca(2) (+) dynamics are impaired showing reduced systolic peak Ca(2) (+), elevated diastolic Ca(2) (+) levels, and prolonged diastolic Ca(2) (+) decay. The recognition that defects in the function of Ca(2) (+) handling proteins are central to the pathogenesis of heart failure has attracted attention to these proteins as potential targets for therapy. Besides pharmacologic interventions including digitalis, ranolazine, levosimendan and others, cardiac gene therapy holds great promise and the recent clinical studies have proven the feasibility of this therapeutic approach. In this review, the rationale underlying modern therapies that modulate intracellular Ca(2) (+) handling for the treatment of human heart failure are presented and discussed.
Indexed as
Identifiers
22688623What 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.