ReviewJournal of molecular and cellular cardiology2016
Thrombospondins in the transition from myocardial infarction to heart failure.
Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Understanding Pathophysiological Complexity of Feline Hypertrophic Cardiomyopathy Using SWATH-MS Plasma Proteomics.Animals : an open access journal from MDPI · 2026Article
- The Role of Thrombospondin-2 in Myocardial Fibrosis.Drug design, development and therapy · 2026Review
- The Proteome Content of Blood Clots Observed Under Different Conditions: Successful Role in Predicting Clot Amyloid(ogenicity).Molecules (Basel, Switzerland) · 2025Review
- Thrombospondin-4 deletion does not exacerbate muscular dystrophy in β-sarcoglycan-deficient and laminin α2 chain-deficient mice.Scientific reports · 2024Article
- Spatiotemporal signaling underlies progressive vascular rarefaction in myocardial infarction.Nature communications · 2023Article
- Novel Targets Regulating the Role of Endothelial Cells and Angiogenesis after Infarction: A RNA Sequencing Analysis.International journal of molecular sciences · 2023Article
- Role of A Single Nucleotide Polymorphism in Thrombospondine 4 Gene in Premature Myocardial Infarction among Population of Southern Iran.ARYA atherosclerosis · 2023Article
- Thrombospondin-2 holds prognostic value and is associated with metastasis and the mismatch repair process in gastric cancer.BMC cancer · 2022Article
- Article
- Fibroblast contributions to ischemic cardiac remodeling.Cellular signalling · 2021Review
- Weighted correlation network bioinformatics uncovers a key molecular biosignature driving the left-sided heart failure.BMC medical genomics · 2020Article
- The Influence of the Extracellular Matrix in Inflammation: Findings from the SPARC-Null Mouse.Anatomical record (Hoboken, N.J. : 2007) · 2020Review
- Effects of thrombospondin-4 on pro-inflammatory phenotype differentiation and apoptosis in macrophages.Cell death & disease · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Defective Flux of Thrombospondin-4 through the Secretory Pathway Impairs Cardiomyocyte Membrane Stability and Causes Cardiomyopathy.Molecular and cellular biology · 2018Article
- Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding.American journal of physiology. Heart and circulatory physiology · 2018Review
- Altered expression of thrombospondin-1/-2 in the cortex and synaptophysin in the hippocampus after middle cerebral artery occlusion and reperfusion.International journal of clinical and experimental pathology · 2018Article
- The Roles of Matricellular Proteins in Oncogenic Virus-Induced Cancers and Their Potential Utilities as Therapeutic Targets.International journal of molecular sciences · 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 1 country.
Funding
Abstract
The heart's reaction to ischemic injury from a myocardial infarction involves complex cross-talk between the extra-cellular matrix (ECM) and different cell types within the myocardium. The ECM functions not only as a scaffold where myocytes beat synchronously, but an active signaling environment that regulates the important post-MI responses. The thrombospondins are matricellular proteins that modulate cell--ECM interactions, functioning as "sensors" that mediate outside-in and inside-out signaling. Thrombospondins are highly expressed during embryonic stages, and although their levels decrease during adult life, can be re-expressed in high quantities in response to cardiac stress including myocardial infarction and heart failure. Like a Swiss-army knife, the thrombospondins possess many tools: numerous binding domains that allow them to interact with other elements of the ECM, cell surface receptors, and signaling molecules. It is through these that the thrombospondins function. In the present review, we provide basic as well as clinical evidence linking the thrombospondin proteins with the post myocardial infarction response, including inflammation, fibrotic matrix remodeling, angiogenesis, as well as myocyte hypertrophy, apoptosis, and contractile dysfunction in heart failure. We will describe what is known regarding the intracellular signaling pathways that are involved with these responses, paving the road for future studies identifying these proteins as therapeutic targets for cardiac disease.
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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.