ArticleAdvances in experimental medicine and biology2021
Connective Tissue Disorders and Cardiovascular Complications: The Indomitable Role of Transforming Growth Factor-β Signaling.
Article in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07495267 (Nutritional Ketosis as a Novel Therapeutic Strategy to Stabilize Chronic Aortic Dissection in Marfan Syndrome), which is not on this map. Cited by 10 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.
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.
Nutritional Ketosis as a Novel Therapeutic Strategy to Stabilize Chronic Aortic Dissection in Marfan Syndrome
Who cites it
10 citing papers in PubMed.
- A personalized home-based exercise training program in children with Marfan and Loeys-Dietz syndromes improves aerobic exercise capacity and health-related quality of life.Orphanet journal of rare diseases · 2026Trial
- The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- The causal role of plasma protein ratios in ulcerative colitis: insights from mendelian randomization and single-cell sequencing.Open medicine (Warsaw, Poland) · 2026Article
- A Family with Meester-Loeys Syndrome Caused by a Novel Missense Variant in theInternational journal of molecular sciences · 2025Article
- The Contribution of Mast Cells to the Regulation of Elastic Fiber Tensometry in the Skin Dermis of Children with Marfan Syndrome.International journal of molecular sciences · 2024Article
- Navigating toward gene therapy in Marfan syndrome: A hope for halting aortic aneurysm.Molecular therapy. Methods & clinical development · 2024Article
- The Metabolic Syndrome, a Human Disease.International journal of molecular sciences · 2024Review
- MEK inhibitors: a promising targeted therapy for cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- TGFβ-2 haploinsufficiency causes early death in mice with Marfan syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Transforming growth factor serum concentrations in patients with proven non-syndromic aortopathy.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Marfan Syndrome (MFS) and Loeys-Dietz Syndrome (LDS) represent heritable connective tissue disorders that segregate with a similar pattern of cardiovascular defects (thoracic aortic aneurysm, mitral valve prolapse/regurgitation, and aortic dilatation with regurgitation). This pattern of cardiovascular defects appears to be expressed along a spectrum of severity in many heritable connective tissue disorders and raises suspicion of a relationship between the normal development of connective tissues and the cardiovascular system. With overwhelming evidence of the involvement of aberrant Transforming Growth Factor-beta (TGF-β) signaling in MFS and LDS, this signaling pathway may represent the common link in the relationship between connective tissue disorders and their associated cardiovascular complications. To further explore this hypothetical link, this chapter will review the TGF-β signaling pathway, the heritable connective tissue syndromes related to aberrant TGF-β signaling, and will discuss the pathogenic contribution of TGF-β to these syndromes with a primary focus on the cardiovascular system.
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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.