ArticleThe American journal of pathology2007
Inactivation of Smad5 in endothelial cells and smooth muscle cells demonstrates that Smad5 is required for cardiac homeostasis.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- SMAD5 as a novel gene for familial pulmonary arterial hypertension.Clinical science (London, England : 1979) · 2025Article
- Exploring Smad5: a review to pave the way for a deeper understanding of the pathobiology of common respiratory diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Novel roles of an intragenic G-quadruplex in controlling microRNA expression and cardiac function.Nucleic acids research · 2021Article
- Specification of BMP Signaling.Cells · 2019Review
- Targeting of Mesenchymal Stromal Cells by Cre-Recombinase Transgenes Commonly Used to Target Osteoblast Lineage Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016Article
- Smad1/5/8 are myogenic regulators of murine and human mesoangioblasts.Journal of molecular cell biology · 2016Article
- SMAD1 and SMAD5 Expression Is Coordinately Regulated by FLI1 and GATA2 during Endothelial Development.Molecular and cellular biology · 2015Article
- Pericytes as targets in hereditary hemorrhagic telangiectasia.Frontiers in genetics · 2015Review
- CHD7 interacts with BMP R-SMADs to epigenetically regulate cardiogenesis in mice.Human molecular genetics · 2014Article
- Genetic polymorphism of SMAD5 is associated with Kawasaki disease.Pediatric cardiology · 2014Article
- Numb family proteins are essential for cardiac morphogenesis and progenitor differentiation.Development (Cambridge, England) · 2014Article
- Epicardial calcineurin-NFAT signals through Smad2 to direct coronary smooth muscle cell and arterial wall development.Cardiovascular research · 2014Article
- Loss of neurotrophin-3 from smooth muscle disrupts vagal gastrointestinal afferent signaling and satiation.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Smooth muscle cell-specific runx2 deficiency inhibits vascular calcification.Circulation research · 2012Article
- Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice.Cell research · 2012Article
- Connective tissue growth factor acts within both endothelial cells and beta cells to promote proliferation of developing beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Altered prostate epithelial development and IGF-1 signal in mice lacking the androgen receptor in stromal smooth muscle cells.The Prostate · 2011Article
- BMP signaling in vascular development and disease.Cytokine & growth factor reviews · 2010Review
- Spatial and temporal regulation of coronary vessel formation by calcineurin-NFAT signaling.Development (Cambridge, England) · 2009Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smads are intracellular signaling proteins that transduce signals elicited by members of the transforming growth factor (TGF)-beta superfamily. Smad5 and Smad1 are highly homologous, and they mediate primarily bone morphogenetic protein (Bmp) signals. We used the Cre-loxP system and Sm22-Cre and Tie-1-Cre mice to study the function of Smad5 in the developing blood vessel wall. Analysis of embryos demonstrated that deletion of Smad5 in endothelial or smooth muscle cells resulted in a normal organization of embryonic and extra-embryonic vasculature. Angiogenic assays performed in adult mice revealed that mutant mice display a comparable angiogenic and vascular remodeling response to control mice. In Sm22-Cre; Smad5(fl/-) mice, Smad5 is also deleted in cardiomyocytes. Echocardiographic analysis on those 9-month-old female mice demonstrated larger left ventricle internal diameters and decreased fractional shortening compared with control littermates without signs of cardiac hypertrophy. The decreased cardiac contractility was associated with a decreased performance in a treadmill experiment. In isolated cardiomyocytes, fractional shortening was significantly reduced compared with control cells. These data demonstrate that restricted deletion of Smad5 in the blood vessel wall results in viable mice. However, loss of Smad5 in cardiomyocytes leads to a mild heart defect.
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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.