ReviewCellular signalling2021
Cross your heart? Collagen cross-links in cardiac health and disease.
Review in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 69 citations in OpenAlex.
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Article
- Ro5-4864, a ligand of the mitochondrial translocator protein, protects against heart failure in mice via regulation of the p62-Keap1-Nrf2 axis.The Journal of physiology · 2026Article
- Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis.Signal transduction and targeted therapy · 2026Article
- Single Antenatal Exposure to Ciclesonide Reduces Long-Term Cardiac Structural and Functional Alterations Compared to Currently Approved Synthetic Corticosteroids.Research square · 2026Article
- Proteomic and degradomic signatures of extracellular matrix remodeling in calcific aortic valve stenosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- ATP7A-fibulin-4 complex delivers copper in the Golgi to activate LOX in renal fibrosis.JCI insight · 2026Article
- Reductions in myocardial interstitial fibrosis are dissociated from LV chamber stiffness in swine with repetitive pressure overload.American journal of physiology. Heart and circulatory physiology · 2026Article
- Integrated transcriptomics and proteomics analysis reveal potential target in pediatric primary restrictive cardiomyopathy.Pediatric research · 2026Article
- Mechanical Modeling of Cardiac Fibrosis With Explicit Spatial Representation of Cellular Structure and Collagen Alignment.Journal of biomechanical engineering · 2026Article
- Composition and Influence of Fibrogenic Niche in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2026Review
- Collagen in Fibrotic Diseases.Sub-cellular biochemistry · 2026Review
- Advanced glycation end products and RAGE signaling in diabetic cardiomyopathy: distinct mechanisms, human evidence, and translational barriers.Frontiers in cardiovascular medicine · 2026Review
- Cardiolipin remodelling in mitochondrial therapeutics: translational evidence chains from elamipretide to emerging strategies.Frontiers in physiology · 2026Review
- Systematic computational assessment of atrial function impairment due to fibrotic remodeling in electromechanical properties.PLoS computational biology · 2025Article
- Extracellular matrix alterations in chronic ischemic cardiomyopathy revealed by quantitative proteomics.JCI insight · 2025Article
- Regulation of neutrophil function by the extracellular matrix.Biochemical Society transactions · 2025Review
- Organ fibrosis: beyond collagen I expression. Fibroblast phenotype and basement membrane proteins.American journal of physiology. Cell physiology · 2025Review
- Thermal tolerance of turbot based on cardiac performance and analysis of molecular regulatory mechanisms.Fish physiology and biochemistry · 2025Article
- Anti-fibrotic, muscle-promoting antibody-drug conjugates for the improvement and treatment of DMD.iScience · 2025Article
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 1 country.
Funding
Abstract
Extracellular matrix (ECM) remodeling occurs in response to various cardiac insults including infarction, pressure overload and dilated myopathies. Each type of remodeling necessitates distinct types of ECM turnover and deposition yet an increase in myocardial fibrillar collagen content is appreciated as a contributing feature to cardiac dysfunction in each of these pathologies. In addition, aging, is also associated with increases in cardiac collagen content. The importance of characterizing differences in ECM composition and processes used by cardiac fibroblasts in the assembly of fibrotic collagen accumulation is critical for the design of strategies to reduce and ultimately regress cardiac fibrosis. Collagen cross-linking is one factor that influences collagen deposition and insolubility with direct implications for tissue properties such as stiffness. In this review, three different types of collagen cross-links shown to be important in cardiac fibrosis will be discussed; those catalyzed by lysyl oxidases, those catalyzed by transglutaminases, and those that result from non-enzymatic modification by the addition of advanced glycation end products. Insight into cellular mechanisms that govern collagen cross-linking in the myocardium will provide novel pathways for exploring new treatments to treat diseases associated with cardiac fibrosis.
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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.