ArticleCell cycle (Georgetown, Tex.)2011
Scleroderma-like properties of skin from caveolin-1-deficient mice: implications for new treatment strategies in patients with fibrosis and systemic sclerosis.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Adipocytes as core drivers of skin aging and novel targets for regeneration.Biogerontology · 2026Review
- [Research progress on cellular metabolic reprogramming in skin fibrosis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Revolutionizing Autoimmune Research: The Role of Caveolin-1.Immunity, inflammation and disease · 2025Review
- The crosstalk of caveolin-1 and autophagy in different diseases.Frontiers in immunology · 2025Review
- STING-STAT6 Signaling Pathway Promotes IL-4Immune network · 2024Article
- Mechanisms of autophagy and their implications in dermatological disorders.Frontiers in immunology · 2024Review
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
- The Role of SOX9 in IGF-II-Mediated Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- The Role of Autophagy and Apoptosis in Affected Skin and Lungs in Patients with Systemic Sclerosis.International journal of molecular sciences · 2023Review
- Mitochondrial DNA copy number in patients with systemic sclerosis.Frontiers in molecular biosciences · 2023Article
- Immunometabolism changes in fibrosis: from mechanisms to therapeutic strategies.Frontiers in pharmacology · 2023Review
- Animal Models of Systemic Sclerosis: Using Nailfold Capillaroscopy as a Potential Tool to Evaluate Microcirculation and Microangiopathy: A Narrative Review.Life (Basel, Switzerland) · 2022Review
- Metformin ameliorates scleroderma via inhibiting Th17 cells and reducing mTOR-STAT3 signaling in skin fibroblasts.Journal of translational medicine · 2021Article
- Engineering Advanced In Vitro Models of Systemic Sclerosis for Drug Discovery and Development.Advanced biology · 2021Review
- Mesenchymal stem cell as a novel approach to systemic sclerosis; current status and future perspectives.Cell regeneration (London, England) · 2020Review
- Understanding Fibrosis in Systemic Sclerosis: Novel and Emerging Treatment Approaches.Current rheumatology reports · 2020Review
- The importance of caveolins and caveolae to dermatology: Lessons from the caves and beyond.Experimental dermatology · 2020Review
- Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Caveolin-1 as a target in prevention and treatment of hypertrophic scarring.NPJ Regenerative medicine · 2019Review
- Caveolin-1 as a pathophysiological factor and target in psoriasis.NPJ aging and mechanisms of disease · 2019Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Caveolin-1 (Cav-1), the principal structural component of caveolae, participates in the pathogenesis of several fibrotic diseases, including systemic sclerosis (SSc). Interestingly, affected skin and lung samples from patients with SSc show reduced levels of Cav-1, as compared to normal skin. In addition, restoration of Cav-1 function in skin fibroblasts from SSc patients reversed their pro-fibrotic phenotype. Here, we further investigated whether Cav-1 mice are a useful pre-clinical model for studying the pathogenesis of SSc. For this purpose, we performed quantitative transmission electron microscopy, as well as biochemical and immuno-histochemical analysis, of the skin from Cav-1 (-/-) null mice. Using these complementary approaches, we now show that skin from Cav-1 null mice exhibits many of the same characteristics as SSc skin from patients, including a decrease in collagen fiber diameter, increased tensile strength, and stiffness, as well as mononuclear cell infiltration. Furthermore, an increase in autophagy/mitophagy was observed in the stromal cells of the dermis from Cav-1 (-/-) mice. These findings suggest that changes in cellular energy metabolism (e.g., a shift towards aerobic glycolysis) in these stromal cells may be a survival mechanism in this "hostile" or pro-inflammatory microenvironment. Taken together, our results demonstrate that Cav-1 (-/-) null mice are a valuable new pre-clinical model for studying scleroderma. Most importantly, our results suggest that inhibition of autophagy and/or aerobic glycolysis may represent a new promising therapeutic strategy for halting fibrosis in SSc patients. Finally, Cav-1 (-/-) null mice are also a pre-clinical model for a "lethal" tumor micro-environment, possibly explaining the link between fibrosis, tumor progression, and cancer metastasis.
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