ReviewBiomedicines2024
Recent Insights into Cellular and Molecular Mechanisms of Defective Angiogenesis in Systemic Sclerosis.
Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mitochondrial Dysregulation and Molecular Signaling in Systemic Sclerosis Cardiac Disease: An Integrative Echocardiographic, Microvascular, and Biomarker Review.International journal of molecular sciences · 2026Review
- Gain of function NOTCH4 variants disrupt angiogenesis in systemic sclerosis.Annals of the rheumatic diseases · 2026Article
- Leveraging experimental vasculature data for high-resolution brain tumor simulations.Biophysical journal · 2026Article
- Mechanisms of fibrotic tissue remodelling: insights from systemic sclerosis.Nature reviews. Rheumatology · 2026Review
- Unveiling Vascular Dynamics: Introducing theBiomedicines · 2025Article
- Decoding vascular dysfunction in systemic sclerosis: from endothelial damage to clinical implications.Current opinion in rheumatology · 2025Review
- Review
- Microvascular Density Analysis of Patients with Trigeminal Herpes Zoster-An Optical Coherence Tomography Angiography Study.Biomedicines · 2025Article
- Immunoglobulins G from Patients with Systemic Sclerosis Modify the Molecular Signatures of Endothelial Cells.RMD open · 2025Article
- Characterization of Circulating Vesicles of Complicated and Uncomplicated Systemic Sclerosis Patients and Their Role in Vascular Dysfunction.International journal of molecular sciences · 2025Article
- Cardiac disease in systemic sclerosis: a narrative review.Archives of medical sciences. Atherosclerotic diseases · 2025Article
- Endothelin-1 as a Candidate Biomarker of Systemic Sclerosis: A GRADE-Assessed Systematic Review and Meta-Analysis With Meta-Regression.Biomarker insights · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In systemic sclerosis (SSc, or scleroderma), defective angiogenesis, clinically manifesting with abnormal capillary architecture and severe capillary reduction, represents a hallmark of early-stage disease, usually preceding the onset of tissue fibrosis, and is caused by several cellular and molecular mechanisms affecting microvascular endothelial cells with different outcomes. Indeed, once damaged, endothelial cells can be dysfunctionally activated, thus becoming unable to undergo angiogenesis and promoting perivascular inflammation. They can also undergo apoptosis, transdifferentiate into profibrotic myofibroblasts, or acquire a senescence-associated secretory phenotype characterized by the release of exosomes and several profibrotic and proinflammatory mediators. In this narrative review, we aimed to give a comprehensive overview of recent studies dealing with the cellular and molecular mechanisms underlying SSc defective angiogenesis and the related endothelial cell dysfunctions, mainly the endothelial-to-mesenchymal transition process. We also discussed potential novel vascular treatment strategies able to restore the angiogenic process and reduce the endothelial-to-mesenchymal transition in this complex 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.