ArticleJCI insight2020
SLIT3 deficiency attenuates pressure overload-induced cardiac fibrosis and remodeling.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- Elevated serum Slit3 independently predicts disease activity and interstitial lung disease in rheumatoid arthritis.Clinics (Sao Paulo, Brazil) · 2026Article
- Slit2-robo signaling regulates angiogenesis and repair following myocardial infarction.Journal of molecular and cellular cardiology · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years.Mechanobiology in medicine · 2025Review
- Identifying Key Biomarkers Related to Immune Response in the Progression of Diabetic Kidney Disease: Mendelian Randomization Combined With Comprehensive Transcriptomics and Single-Cell Sequencing Analysis.Journal of inflammation research · 2025Article
- Cardiac fibroblasts: answering the call.American journal of physiology. Heart and circulatory physiology · 2024Review
- Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy.Circulation research · 2024Article
- Plasma fibroblast activation protein is decreased in acute heart failure despite cardiac tissue upregulation.Journal of translational medicine · 2024Article
- SLIT3 promotes cardiac fibrosis and differentiation of cardiac fibroblasts by RhoA/ROCK1 signaling pathway.Iranian journal of basic medical sciences · 2024Article
- SLIT3-mediated fibroblast signaling: a promising target for antifibrotic therapies.American journal of physiology. Heart and circulatory physiology · 2023Review
- Role of the SLIT-ROBO signaling pathway in renal pathophysiology and various renal diseases.Frontiers in physiology · 2023Review
- Single-nucleus ribonucleic acid-sequencing and spatial transcriptomics reveal the cardioprotection of Shexiang Baoxin Pill (SBP) in mice with myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2023Article
- Analysis of Copy Number Variation in the Whole Genome of Normal-Haired and Long-Haired Tianzhu White Yaks.Genes · 2022Article
- Identification of recurrent variants implicated in disease in bicuspid aortic valve patients through whole-exome sequencing.Human genomics · 2022Article
- Pathogenic variants damage cell composition and single cell transcription in cardiomyopathies.Science (New York, N.Y.) · 2022Article
- Distinct Adipogenic and Fibrogenic Differentiation Capacities of Mesenchymal Stromal Cells from Pancreas and White Adipose Tissue.International journal of molecular sciences · 2022Article
- Whole-genome re-sequencing association study on yearling wool traits in Chinese fine-wool sheep.Journal of animal science · 2021Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
In pulmonary hypertension and certain forms of congenital heart disease, ventricular pressure overload manifests at birth and is an obligate hemodynamic abnormality that stimulates myocardial fibrosis, which leads to ventricular dysfunction and poor clinical outcomes. Thus, an attractive strategy is to attenuate the myocardial fibrosis to help preserve ventricular function. Here, by analyzing RNA-sequencing databases and comparing the transcript and protein levels of fibrillar collagen in WT and global-knockout mice, we found that slit guidance ligand 3 (SLIT3) was present predominantly in fibrillar collagen-producing cells and that SLIT3 deficiency attenuated collagen production in the heart and other nonneuronal tissues. We then performed transverse aortic constriction or pulmonary artery banding to induce left and right ventricular pressure overload, respectively, in WT and knockout mice. We discovered that SLIT3 deficiency abrogated fibrotic and hypertrophic changes and promoted long-term ventricular function and overall survival in both left and right ventricular pressure overload. Furthermore, we found that SLIT3 stimulated fibroblast activity and fibrillar collagen production, which coincided with the transcription and nuclear localization of the mechanotransducer yes-associated protein 1. These results indicate that SLIT3 is important for regulating fibroblast activity and fibrillar collagen synthesis in an autocrine manner, making it a potential therapeutic target for fibrotic diseases, especially myocardial fibrosis and adverse remodeling induced by persistent afterload elevation.
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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.