ReviewFuture cardiology2015
Cardiomyocytes, endothelial cells and cardiac fibroblasts: S100A1's triple action in cardiovascular pathophysiology.
Review in Future cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 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
10 citing papers in PubMed, 21 citations in OpenAlex.
- S100A1's single cysteine is an indispensable redox switch for the protection against diastolic calcium waves in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2024Article
- Identification of recurrent variants implicated in disease in bicuspid aortic valve patients through whole-exome sequencing.Human genomics · 2022Article
- Adeno-associated viral (AAV) vector-mediated therapeutics for diabetic cardiomyopathy - current and future perspectives.Clinical science (London, England : 1979) · 2021Review
- Therapeutic Effects of Traditional Chinese Medicine on Cardiovascular Diseases: the Central Role of Calcium Signaling.Frontiers in pharmacology · 2021Review
- Arginine and Endothelial Function.Biomedicines · 2020Review
- Leveraging Signaling Pathways to Treat Heart Failure With Reduced Ejection Fraction.Circulation research · 2019Review
- Patients with systemic sclerosis-associated pulmonary arterial hypertension express a genomic signature distinct from patients with interstitial lung disease.Journal of scleroderma and related disorders · 2018Article
- Molecular tissue changes in early myocardial ischemia: from pathophysiology to the identification of new diagnostic markers.International journal of legal medicine · 2018Review
- Inhibition of cardiac CaMKII to cure heart failure: step by step towards translation?Basic research in cardiology · 2016Article
- Cardiac gene therapy: are we there yet?Gene therapy · 2016Review
Corrections and comments
- Erratum issuedErratum.2015
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Over the past decade, basic and translational research delivered comprehensive evidence for the relevance of the Ca(2+)-binding protein S100A1 in cardiovascular diseases. Aberrant expression levels of S100A1 surfaced as molecular key defects, driving the pathogenesis of chronic heart failure, arterial and pulmonary hypertension, peripheral artery disease and disturbed myocardial infarction healing. Loss of intracellular S100A1 renders entire Ca(2+)-controlled networks dysfunctional, thereby leading to cardiomyocyte failure and endothelial dysfunction. Lack of S100A1 release in ischemic myocardium compromises cardiac fibroblast function, entailing impaired damage healing. This review focuses on molecular pathways and signaling cascades regulated by S100A1 in cardiomyocytes, endothelial cells and cardiac fibroblasts in order to provide an overview of our current mechanistic understanding of S100A1's action in cardiovascular pathophysiology.
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.