ArticleCirculation research2010
Thrombospondin-4 regulates vascular inflammation and atherogenesis.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Understanding Tendons: Lessons from Transgenic Mouse Models.Stem cells and development · 2018Pooled it
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- Early alveolar molecular signatures after cardiopulmonary resuscitation: a bronchoalveolar lavage (BALF) proteomic study in swine.Resuscitation plus · 2026Article
- Review
- Thrombospondin-4 drives lymphangiogenesis through cooperation with VEGF-C in human bladder cancer.International journal of medical sciences · 2026Article
- Hepatic steatosis in postmenopausal women is characterized by distinct serum extracellular vesicle proteomic signatures.BMC medicine · 2025Article
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Brown remodeling of white adipose tissue protects against abdominal aortic aneurysm via batokine FSTL1.EMBO molecular medicine · 2025Article
- Fibroblast-specific TGF-β signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice.Cardiovascular research · 2024Article
- CardioAtlas: deciphering the single-cell transcriptome landscape in cardiovascular tissues and diseases.Biomarker research · 2024Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- The role and mechanism of thrombospondin-4 in pulmonary arterial hypertension associated with congenital heart disease.Respiratory research · 2024Article
- Thrombospondin-4 deletion does not exacerbate muscular dystrophy in β-sarcoglycan-deficient and laminin α2 chain-deficient mice.Scientific reports · 2024Article
- The molecular mechanism of thrombospondin family members in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Unraveling the Role of Sex in Endothelial Cell Dysfunction: Evidence From Lineage Tracing Mice and Cultured Cells.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- PRDM16 deficiency in vascular smooth muscle cells aggravates abdominal aortic aneurysm.JCI insight · 2023Article
- Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction.JCI insight · 2023Article
- Plasma proteomics identifies CRTAC1 as a biomarker for osteoarthritis severity and progression.Rheumatology (Oxford, England) · 2023Article
- Gene expression profile of placentomes and clinical parameters in the cows with retained placenta.BMC genomics · 2022Article
- Matricellular proteins in cutaneous wound healing.Frontiers in cell and developmental biology · 2022Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleThrombospondin (TSP)-4 is an extracellular protein that has been linked to several cardiovascular pathologies. However, a role for TSP-4 in vascular wall biology remains unknown.
objectiveWe have examined the effects of TSP-4 gene (Thbs4) knockout on the development of atherosclerotic lesions in ApoE(-/-) mice. METHODS AND
resultsDeficiency in TSP-4 reduced atherosclerotic lesions: at 20 weeks of age, the size of the aortic root lesions in Thbs4(-/-)/ApoE(-/-) mice was decreased by 48% in females and by 39% in males on chow diets; in mice on Western diets, lesions in the descending aorta were reduced by 30% in females and 33% in males. In ApoE(-/-) mice, TSP-4 was abundant in vessel areas prone to lesion development and in the matrix of the lesions themselves. TSP-4 deficiency reduced the number of macrophages in lesions in all groups by ≥ 2-fold. In addition, TSP-4 deficiency reduced endothelial cell activation (expression of surface adhesion molecules) and other markers of inflammation in the vascular wall (decreased production of monocyte chemoattractant protein-1 and activation of p38). In vitro, both the adhesion and migration of wild-type macrophages increased in the presence of purified recombinant TSP-4 in a dose-dependent manner (up to 7- and 4.7-fold, respectively). These responses led to p38-MAPkinase activation and were dependent on β(2) and β(3) integrins, which recognize TSP-4 as a ligand.
conclusionsTSP-4 is abundant in atherosclerotic lesions and in areas prone to development of lesions and may influence the recruitment of macrophages by activating endothelial cells and directly interacting with macrophages to increase their adhesion and migration. Our observations suggest an important role for this matricellular protein in the local regulation of inflammation associated with atherogenesis.
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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.