ReviewFEBS letters2012
Matrix-dependent perturbation of TGFβ signaling and disease.
Review in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 126 citations in OpenAlex.
- Smad3 deficiency attenuates disease severity in a zebrafish model for Smad6-related aortic disease.Angiogenesis · 2026Article
- FGF12 induces aberrant mechanosignaling in aortic smooth muscle cells during thoracic aortic aneurysm formation in Marfan syndrome mice.Experimental & molecular medicine · 2026Article
- Hemodynamic forces prevent myxomatous valve disease in mice through KLF2/4 signaling.The Journal of clinical investigation · 2025Article
- Tissue Mechanics and Hedgehog Signaling Crosstalk as a Key Epithelial-Stromal Interplay in Cancer Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The comprehensive study on the role of POSTN in fetal congenital heart disease and clinical applications.Journal of translational medicine · 2023Article
- Therapeutic Strategies to Overcome Fibrotic Barriers to Nanomedicine in the Pancreatic Tumor Microenvironment.Cancers · 2023Review
- Ageing of skeletal muscle extracellular matrix and mitochondria: finding a potential link.Annals of medicine · 2023Review
- Embryonic Heterogeneity of Smooth Muscle Cells in the Complex Mechanisms of Thoracic Aortic Aneurysms.Genes · 2022Review
- Cysteine-rich domain of type III collagen N-propeptide inhibits fibroblast activation by attenuating TGFβ signaling.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Decellularized extracellular matrix mediates tissue construction and regeneration.Frontiers of medicine · 2022Review
- Annuloaortic ectasia in a four-month-old male Newfoundland dog: long-term follow-up and immunofluorescent study.The veterinary quarterly · 2021Article
- POGLUT2 and POGLUT3 O-glucosylate multiple EGF repeats in fibrillin-1, -2, and LTBP1 and promote secretion of fibrillin-1.The Journal of biological chemistry · 2021Article
- Recurrent germline mutations as genetic markers for aortic root dilatation in bicuspid aortic valve patients.Heart and vessels · 2021Article
- Proof-of-Concept: Antisense Oligonucleotide Mediated Skipping of Fibrillin-1 Exon 52.International journal of molecular sciences · 2021Article
- Progressive Microstructural Deterioration Dictates Evolving Biomechanical Dysfunction in the Marfan Aorta.Frontiers in cardiovascular medicine · 2021Article
- Reactive Oxygen Species and Oxidative Stress in the Pathogenesis and Progression of Genetic Diseases of the Connective Tissue.Antioxidants (Basel, Switzerland) · 2020Review
- Stem cell derived extracellular vesicles for vascular elastic matrix regenerative repair.Acta biomaterialia · 2020Article
- The expanding phenotypes of cohesinopathies: one ring to rule them all!Cell cycle (Georgetown, Tex.) · 2019Review
- Review
- Skin fibroblasts of patients with geleophysic dysplasia due to FBN1 mutations have lysosomal inclusions and losartan improves their microfibril deposition defect.Molecular genetics & genomic medicine · 2019Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Transforming growth factor beta (TGFβ) is a multipotent cytokine that is sequestered in the extracellular matrix (ECM) through interactions with a number of ECM proteins. The ECM serves to concentrate latent TGFβ at sites of intended function, to influence the bioavailability and/or function of TGFβ activators, and perhaps to regulate the intrinsic performance of cell surface effectors of TGFβ signal propagation. The downstream consequences of TGFβ signaling cascades in turn provide feedback modulation of the ECM. This review covers recent examples of how genetic mutations in constituents of the ECM or TGFβ signaling cascade result in altered ECM homeostasis, cellular performance and ultimately disease, with an emphasis on emerging therapeutic strategies that seek to capitalize on this refined mechanistic understanding.
Indexed as
Identifiers
What OpenQuestion holds
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.