ArticleCirculation research2019
Heparan Sulfate-Editing Extracellular Sulfatases Enhance VEGF Bioavailability for Ischemic Heart Repair.
Article in Circulation research, 2019. 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 40 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.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
- Sulf1 regulates inflammation via modulation of TGF-β dependent epicardial activation.EMBO reports · 2026Article
- A sulfated chitosan-driven immune-ECM reprogramming strategy to break the vicious cycle of aged wound healing.Bioactive materials · 2026Article
- Regulated HSPG Signaling Directs Epicardial Behavior to Support Cardiac Formation.Circulation research · 2026Article
- Single cell transcriptomic landscape of adult and pediatric non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Human iPSC-derived cardiac-specific extracellular matrix scaffolds for cardiomyocyte maturation and post-myocardial infarction repair.Bioactive materials · 2026Article
- SULF1 and EPB41L3: Potential Biomarkers of Acute Myocardial Infarction and the Vascular Inflammatory Milieu.Journal of inflammation research · 2026Article
- Elucidating the multifaceted role and therapeutic potential of Sulf-2 in human tumor biology.Biomarkers in medicine · 2025Review
- THE INTERACTION BETWEEN ANTITHROMBIN AND ENDOTHELIAL HEPARAN SULFATE MITIGATES PULMONARY THROMBOINFLAMMATION AFTER TRAUMA AND HEMORRHAGIC SHOCK.Shock (Augusta, Ga.) · 2025Article
- Developments in Extracellular Matrix-Based Angiogenesis Therapy for Ischemic Heart Disease: A Review of Current Strategies, Methodologies and Future Directions.Biotech (Basel (Switzerland)) · 2025Review
- SULF1's Role in Endothelial Senescence and Atherosclerosis: Insights from Single-Cell and Bulk Transcriptomics.Journal of inflammation research · 2025Article
- Harnessing the regenerative potential of interleukin11 to enhance heart repair.Nature communications · 2024Article
- Si and Zn dual ions upregulate the osteogenic differentiation of mBMSCs: mRNA transcriptomic sequencing analysis.Journal of materials science. Materials in medicine · 2024Article
- Article
- The extracellular heparan sulfatase SULF2 limits myeloid IFNβ signaling and Th17 responses in inflammatory arthritis.Cellular and molecular life sciences : CMLS · 2024Article
- Harnessing the regenerative potential ofbioRxiv : the preprint server for biology · 2024Article
- Treatment with αvβ3-integrin-specific 29P attenuates pressure-overload induced cardiac remodelling after transverse aortic constriction in mice.Journal of molecular and cellular cardiology plus · 2024Article
- Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair.Nature cardiovascular research · 2024Article
- Left ventricle function and post-transcriptional events with exercise training in pigs.PloS one · 2024Article
- Spatiotemporal signaling underlies progressive vascular rarefaction in myocardial infarction.Nature communications · 2023Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleMechanistic insight into the inflammatory response after acute myocardial infarction may inform new molecularly targeted treatment strategies to prevent chronic heart failure.
objectiveWe identified the sulfatase SULF2 in an in silico secretome analysis in bone marrow cells from patients with acute myocardial infarction and detected increased sulfatase activity in myocardial autopsy samples. SULF2 (Sulf2 in mice) and its isoform SULF1 (Sulf1) act as endosulfatases removing 6- METHODS AND
resultsBoth Sulfs were dynamically upregulated after coronary artery ligation in mice, attaining peak expression and activity levels during the first week after injury. Sulf2 was expressed by monocytes and macrophages, Sulf1 by endothelial cells and fibroblasts. Infarct border zone capillarization was impaired, scar size increased, and cardiac dysfunction more pronounced in mice with a genetic deletion of either Sulf1 or Sulf2. Studies in bone marrow-chimeric Sulf-deficient mice and Sulf-deficient cardiac endothelial cells established that inflammatory cell-derived Sulf2 and endothelial cell-autonomous Sulf1 promote angiogenesis. Mechanistically, both Sulfs reduced HS sulfation in the infarcted myocardium, thereby diminishing Vegfa (vascular endothelial growth factor A) interaction with HS. Along this line, both Sulfs rendered infarcted mouse heart explants responsive to the angiogenic effects of HS-binding Vegfa
conclusionsThese findings establish HS-editing Sulfs as critical inducers of postinfarction angiogenesis and identify HS sulfation as a therapeutic target for ischemic tissue repair.
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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.