AI Article Synopsis
- - The study identifies that insulin and TGF-β signaling pathways work together through a protein called short gastrulation (sog) to influence the remodeling of the extracellular matrix (ECM) in fat tissue of healthy animals.
- - In animals with tumors, sog also affects TGF-β signaling, leading to increased ECM accumulation in the fat body, which negatively impacts muscle health by depleting essential ECM proteins.
- - The research suggests that enhancing insulin signaling, blocking TGF-β signaling, or adjusting ECM levels through certain proteins can help counteract the muscle wasting seen in cancer patients, emphasizing the role of adipose ECM remodeling in cancer cachexia.
Article Abstract
In this study, we found that in the adipose tissue of wildtype animals, insulin and TGF-β signalling converge via a BMP antagonist short gastrulation (sog) to regulate ECM remodelling. In tumour bearing animals, Sog also modulates TGF-β signalling to regulate ECM accumulation in the fat body. TGF-β signalling causes ECM retention in the fat body and subsequently depletes muscles of fat body-derived ECM proteins. Activation of insulin signalling, inhibition of TGF-β signalling, or modulation of ECM levels via SPARC, Rab10 or Collagen IV in the fat body, is able to rescue tissue wasting in the presence of tumour. Together, our study highlights the importance of adipose ECM remodelling in the context of cancer cachexia.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10702797 | PMC |
| http://dx.doi.org/10.15252/embr.202357695 | DOI Listing |
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