ReviewGene therapy2012
Targeting S100A1 in heart failure.
Review in Gene therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 52 citations in OpenAlex.
- Combination S100A1 and ARC gene therapy as a treatment for Duchenne muscular dystrophy cardiomyopathy.JCI insight · 2026Article
- Amelioration of cisplatin-induced myocardial injury by nanocurcumin through antioxidant, anti-inflammatory, and calcium regulatory mechanisms.Journal of molecular histology · 2025Article
- Targeting Calcium Regulation for Heart Failure and Arrhythmia Therapeutics: A Critical Review.Circulation · 2025Review
- Transcriptomic Signature of Frailty in Older Patients With Cardiovascular Disease Undergoing Cardiac Surgery or TAVI.Journal of cachexia, sarcopenia and muscle · 2025Article
- S100A1ct: A Synthetic Peptide Derived From S100A1 Protein Improves Cardiac Performance and Survival in Preclinical Heart Failure Models.Circulation · 2025Article
- PMEL is involved in snake colour pattern transition from blotches to stripes.Nature communications · 2024Article
- 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
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023Review
- Lineage-specific regulatory changes in hypertrophic cardiomyopathy unraveled by single-nucleus RNA-seq and spatial transcriptomics.Cell discovery · 2023Article
- Changes in extracellular matrix in failing human non-ischemic and ischemic hearts with mechanical unloading.Journal of molecular and cellular cardiology · 2022Article
- Single-cell RNA-seq reveals cellular heterogeneity from deep fascia in patients with acute compartment syndrome.Frontiers in immunology · 2022Article
- Article
- Adeno-associated viral (AAV) vector-mediated therapeutics for diabetic cardiomyopathy - current and future perspectives.Clinical science (London, England : 1979) · 2021Review
- Friend or Foe: S100 Proteins in Cancer.Cancers · 2020Review
- Liposomal Resveratrol and/or Carvedilol Attenuate Doxorubicin-Induced Cardiotoxicity by Modulating Inflammation, Oxidative Stress and S100A1 in Rats.Antioxidants (Basel, Switzerland) · 2020Article
- Targeting CaFrontiers in physiology · 2020Review
- In-depth proteomic profiling of left ventricular tissues in human end-stage dilated cardiomyopathy.Oncotarget · 2017Article
- Concise Review: Mending a Broken Heart: The Evolution of Biological Therapeutics.Stem cells (Dayton, Ohio) · 2017Review
- S100 Proteins As an Important Regulator of Macrophage Inflammation.Frontiers in immunology · 2017Review
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 at 2 institutions in 2 countries.
Funding
Abstract
Heart failure (HF) is the common endpoint of many cardiovascular diseases with a 1-year survival rate of about 50% in advanced stages. Despite increasing survival rates in the past years, current standard therapeutic strategies are far away from being optimal. For this reason, the concept of cardiac gene therapy for the treatment of HF holds great potential to improve disease progression, as it specifically targets key pathologies of diseased cardiomyocytes (CM). The small calcium (Ca(2+))-binding protein S100A1 presents a promising target for cardiac gene therapy, as it has been identified as a central regulator of cardiac performance and the Ca(2+)-driven network within CM. S100A1 was shown to regulate sarcoplasmic reticulum, sarcomere and mitochondrial function by modulating target protein activity. Furthermore, deranged S100A1 expression has been linked to HF in human ischemic and dilated cardiomyopathies as well as in various HF animal models. Proof-of-concept studies in small and large animal models as wells as in human failing CM could demonstrate feasibility and efficacy of S100A1 genetically targeted therapy. This review summarizes the developmental steps of S100A1 gene therapy for the implementation into first human clinical trials.
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.