ArticleOncogene2019
Mitochondrial dysfunction is a key determinant of the rare disease lymphangioleiomyomatosis and provides a novel therapeutic target.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Stimulator of interferon genes (STING) in renal tumors: Biological bases, diagnostic relevance, and predictive potential.Histology and histopathology · 2026Review
- Stimulator of interferon genes immunohistochemical expression in the spectrum of extrarenal perivascular epithelioid cell lesions.Scientific reports · 2025Article
- Exploring the uncharted role of cell senescence in rare diseases.Orphanet journal of rare diseases · 2025Review
- EndothelialResearch square · 2024Article
- Tuberous Sclerosis Complex and the kidneys: what nephrologists need to know.Jornal brasileiro de nefrologia · 2024Review
- Deoxyguanosine kinase deficiency and recurrent spontaneous pneumothorax: a case report.Journal of medical case reports · 2023Article
- Prdx5 in the Regulation of Tuberous Sclerosis Complex Mutation-Induced Signaling Mechanisms.Cells · 2023Article
- Histamine signaling and metabolism identify potential biomarkers and therapies for lymphangioleiomyomatosis.EMBO molecular medicine · 2021Article
- Activated p53 in the anti-apoptotic milieu of tuberous sclerosis gene mutation induced diseases leads to cell death if thioredoxin reductase is inhibited.Apoptosis : an international journal on programmed cell death · 2021Article
- Normalization of Enzyme Expression and Activity Regulating Vitamin A Metabolism Increases RAR-Beta Expression and Reduces Cellular Migration and Proliferation in Diseases Caused by Tuberous Sclerosis Gene Mutations.Frontiers in oncology · 2021Article
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Authors and funding
10 authors.
Funding
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Abstract
Lymphangioleiomyomatosis (LAM) is a rare and progressive systemic disease affecting mainly young women of childbearing age. A deterioration in lung function is driven by neoplastic growth of atypical smooth muscle-like LAM cells in the pulmonary interstitial space that leads to cystic lung destruction and spontaneous pneumothoraces. Therapeutic options for preventing disease progression are limited and often end with lung transplantation temporarily delaying an inevitable decline. To identify new therapeutic strategies for this crippling orphan disease, we have performed array based and metabolic molecular analysis on patient-derived cell lines. Our results point to the conclusion that mitochondrial biogenesis and mitochondrial dysfunction in LAM cells provide a novel target for treatment.
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