ArticleThe American journal of pathology2007
Caveolin-1(-/-)- and caveolin-2(-/-)-deficient mice both display numerous skeletal muscle abnormalities, with tubular aggregate formation.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis of expression signatures of muscle atrophy: gene interaction networks in early and late stages.BMC genomics · 2008Pooled it
- Biomarkers of Sarcopenia: Current Status and Future Perspectives.Aging medicine (Milton (N.S.W)) · 2026Review
- Review
- Disrupting lipid homeostasis with CAV2 in OSCC triggers apoptosis, lipolysis, and mitochondrial dysfunction by transcriptional repression of PPARγ.Cell & bioscience · 2025Article
- Downregulation of Caveolae-Associated Proteins in Psoriasis: A Case Series Study.JID innovations : skin science from molecules to population health · 2024Article
- Progressive reorganization of mitochondrial apparatus in aging skeletal muscle of naked mole rats (Aging · 2021Article
- GFPT1 deficiency in muscle leads to myasthenia and myopathy in mice.Human molecular genetics · 2018Article
- An integrated analysis revealed different microRNA-mRNA profiles during skeletal muscle development between Landrace and Lantang pigs.Scientific reports · 2017Article
- Muscle injury, impaired muscle function and insulin resistance in Chromogranin A-knockout mice.The Journal of endocrinology · 2017Article
- Attenuated rapid onset vasodilation with greater force production in skeletal muscle of caveolin-2-/- mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- Elucidation of caveolin 1 both as a tumor suppressor and metastasis promoter in light of epigenetic modulators.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Primary over-expression of AβPP in muscle does not lead to the development of inclusion body myositis in a new lineage of the MCK-AβPP transgenic mouse.International journal of experimental pathology · 2013Article
- Congenital myasthenic syndrome with tubular aggregates caused by GFPT1 mutations.Journal of neurology · 2012Article
- Altered mitochondrial function and metabolic inflexibility associated with loss of caveolin-1.Cell metabolism · 2012Article
- Sequential stages in the age-dependent gradual formation and accumulation of tubular aggregates in fast twitch muscle fibers: SERCA and calsequestrin involvement.Age (Dordrecht, Netherlands) · 2012Article
- Caveolins in rhabdomyosarcoma.Journal of cellular and molecular medicine · 2011Review
- Caveolin-2 is a negative regulator of anti-proliferative function and signaling of transforming growth factor-β in endothelial cells.American journal of physiology. Cell physiology · 2011Article
- Mice lacking TR4 nuclear receptor develop mitochondrial myopathy with deficiency in complex I.Molecular endocrinology (Baltimore, Md.) · 2011Article
- New glimpses of caveolin-1 functions in embryonic development and human diseases.Frontiers in biology · 2011Review
- Novel insights into the role of caveolin-2 in cell- and tissue-specific signaling and function.Biochemistry research international · 2011Article
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10 authors.
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Abstract
Here, we examine the role of "non-muscle" caveolins (Cav-1 and Cav-2) in skeletal muscle biology. Our results indicate that skeletal muscle fibers from male Cav-1(-/-) and Cav-2(-/-) mice show striking abnormalities, such as tubular aggregates, mitochondrial proliferation/aggregation, and increased numbers of M-cadherin-positive satellite cells. Notably, these skeletal muscle defects were more pronounced with increasing age. Because Cav-2-deficient mice displayed normal expression levels of Cav-1, whereas Cav-1-null mice exhibited an almost complete deficiency in Cav-2, these skeletal muscle abnormalities seem to be due to loss of Cav-2. Thus, Cav-2(-/-) mice represent a novel animal model-and the first genetically well-defined mouse model-that can be used to study the pathogenesis of tubular aggregate formation, which remains a poorly understood age-related skeletal muscle abnormality. Finally, because Cav-1 and Cav-2 were not expressed within mature skeletal myofibers, our results indicate that development of these abnormalities probably originates in stem/precursor cells, such as satellite cells or myoblasts. Consistent with this hypothesis, skeletal muscle isolated from male Cav-3(-/-) mice did not show any of these abnormalities. As such, this is the first study linking stem cells with the genesis of these intriguing muscle defects.
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