ArticleScience signaling2022
Cross-talk between TSC2 and the extracellular matrix controls pulmonary vascular proliferation and pulmonary hypertension.
Article in Science signaling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Autophagy-Targeted Vascular Remodeling in Pulmonary Arterial Hypertension: Molecular Mechanisms and Therapeutic Perspectives.Journal of cardiovascular development and disease · 2026Review
- The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- ALDOB K87 lactylation drives mitochondrial fission and metabolic reprogramming in pulmonary hypertension.Communications biology · 2026Article
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Can Sirtuin 1 Serve as a Therapeutic Target in Pulmonary Arterial Hypertension? A Comprehensive Review.Molecules (Basel, Switzerland) · 2025Review
- Will Stub1 Be the Next Target for Pulmonary Hypertension Therapy Development?American journal of respiratory cell and molecular biology · 2025Article
- The dual role of mTOR signaling in lung development and adult lung diseases.Cell & bioscience · 2025Review
- The nitrofen/bisdiamine murine model of congenital diaphragmatic hernia has a pulmonary hypertension vascular phenotype consistent with human CDH.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Exploring Integrin α5β1 as a Potential Therapeutic Target for Pulmonary Arterial Hypertension: Insights From Comprehensive Multicenter Preclinical Studies.Circulation · 2025Article
- Class III Phosphatidylinositol-3 Kinase/Vacuolar Protein Sorting 34 in Cardiovascular Health and Disease.Journal of cardiovascular translational research · 2025Review
- Channeling Hope in the Expanding Landscape of Therapy for Pulmonary Hypertension: Potential Role for Piezo2.Hypertension (Dallas, Tex. : 1979) · 2025Article
- EEPD1 regulates inflammation and endothelial apoptosis in atherosclerosis through KLF4-EEPD1-ERK axis.Clinical and translational medicine · 2025Article
- Pulmonary Hypertension: Pharmacological and Non-Pharmacological Therapies.Life (Basel, Switzerland) · 2024Review
- Hyperactive mTORC1 in lung mesenchyme induces endothelial cell dysfunction and pulmonary vascular remodeling.The Journal of clinical investigation · 2023Article
- Pulmonary Hypertension: A Contemporary Review.American journal of respiratory and critical care medicine · 2023Review
- Characterization of a spontaneous mouse model of mild, accelerated aging via ECM degradation in emphysematous lungs.Scientific reports · 2023Article
- UnWNTing the Heart: Targeting WNT Signaling in Pulmonary Arterial Hypertension.Circulation research · 2023Article
- The Pharmacological Efficacy of Baicalin in Inflammatory Diseases.International journal of molecular sciences · 2023Review
- GATA6 coordinates cross-talk between BMP10 and oxidative stress axis in pulmonary arterial hypertension.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Increased proliferation and survival of cells in small pulmonary arteries (PAs) drive pulmonary arterial hypertension (PAH). Because cell growth mediated by the mTOR-containing mTORC1 complex is inhibited by tuberous sclerosis complex 2 (TSC2), we investigated the role of this GTPase-activating protein in PAH pathology. TSC2 abundance was decreased in remodeled small PAs and PA vascular smooth muscle cells (PAVSMCs) from patients with PAH or from rodent pulmonary hypertension (PH) models, as well as PAVSMCs maintained on substrates that reproduced pathology-induced stiffness. Accordingly, mice with smooth muscle-specific reduction in TSC2 developed PH. At the molecular level, decreased TSC2 abundance led to stiffness-induced PAVSMC proliferation, increased abundance of the mechanosensitive transcriptional coactivators YAP/TAZ, and enhanced mTOR kinase activity. Moreover, extracellular matrix (ECM) produced by TSC2-deficient PAVSMCs stimulated the proliferation of nondiseased PA adventitial fibroblasts and PAVSMCs through fibronectin and its receptor, the α
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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 Socratic graph.