ArticleStem cells translational medicine2025
TGFBR3 dependent mechanism of TGFB2 in smooth muscle cell differentiation and implications for TGFB2-related aortic aneurysm.
Article in Stem cells translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- Age-stratified genomic analyses reveal population-specific genetic determinants of exceptional longevity in Taiwan.GeroScience · 2026Article
- Coronary artery disease risk gene PRDM16 regulates smooth muscle homeostasis.Journal of molecular and cellular cardiology · 2026Article
- Multi-trait and Gene-Based Analyses Identify Genetic Variants Associated with Spontaneous Coronary Artery Dissection.medRxiv : the preprint server for health sciences · 2026Article
- Construction of a Three-Dimensional Calcific Aortic Valve Disease Model Using Human iPSC-Derived Valvular Interstitial Cells.Stem cell reviews and reports · 2026Article
- CRISPR/Cas9-mediated CH2 deletion of Fel d1 triggers transcriptomic reprogramming and disease-associated pathways in feline cells.Frontiers in cell and developmental biology · 2025Article
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Abstract
introductionPathogenic variants in canonical transforming growth factor β (TGFβ) signaling genes predispose patients to thoracic aortic aneurysm and dissection (TAAD), predominantly in aortic root. Although TAAD pathogenesis associated with TGFβ receptor defects is well characterized, distinct and redundant mechanisms of TGFβ isoforms in TAAD incidence and severity remain elusive.
objectiveHere we examined the biological role of TGFB2 in smooth muscle cell (SMC) differentiation and investigated how TGFB2 defects can lead to regional TAAD manifestations.
methodsTo characterize the role of TGFB2 in SMC differentiation and function, we employed human-induced pluripotent stem cell (hiPSC)-derived SMC differentiation, CRISPR/Cas9 gene editing, three-dimensional SMC constructs, and human aortic tissue samples.
resultsDespite the similar effects of different TGFβ isoforms on hiPSC-derived SMC differentiation, siRNA experiments revealed that TGFB2 distinctively displays TGFBR3 dependence for signal transduction, an understudied TGFβ receptor in TAAD. Molecular evaluation of different thoracic aorta regions suggested TGFB2 and TGFBR3 enrichment in the aortic root tunica media. TGFB2 haploinsufficiency (TGFB2KO/+) and TGFB2 neutralization impaired the differentiation of second heart field-derived SMCs. TGFBR3KO/KO prevented the molecular rescue of TGFB2KO/+ by TGFB2 supplementation indicating the involvement of TGFBR3 in TGFB2-mediated SMC differentiation. Lastly, a missense TGFB2 variant (TGFB2G276R/+) caused mechanical defects in SMC tissue ring constructs that were rescued by TGFB2 supplementation or genetic correction.
conclusionOur data suggests the distinct regulation and action of TGFB2 in SMCs populating the aortic root, while redundant activities of TGFβ isoforms provide implications about the milder TAAD aggressiveness of pathogenic TGFB2 variants.
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