What is it about?
This manuscript shows that hepatic stellate cells carrying the genetic variant of PNPLA3 show accumulation of Free Cholesterol and Total cholesterol, in addition to increased pro-fibrogenic features. Basically, we demonstrated that LXR signaling controls Cholesterol homeostasis and it is decreased in these cells. Moreover, the diminished LXR activity is controlled upstream by PPARgamma. HSC treated with the synthetic agonist of LXR (T09) are able to recover the altered phenotype as well as wild type PNPLA3 HSC, while the agonist of PPARgamma, ROSI, is not efficient in HSC with the I148M variant.
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Why is it important?
This manuscript provides important informations regarding a possible therapeutic approach using LXR agonists to block fibrogenesis development in patients with the PNPLA3 genetic variant.
Perspectives
This manuscript might serve to increase the knowledge on how LXR is modulated and its impact during fibrogenesis and HSC activation. Therefore, LXR might serve as target under other circumstances.
PhD Francesca Virginia Bruschi
Medical University of Vienna
Read the Original
This page is a summary of: PNPLA3
I148M Variant Impairs Liver X Receptor Signaling and Cholesterol Homeostasis in Human Hepatic Stellate Cells, Hepatology Communications, July 2019, Wiley,
DOI: 10.1002/hep4.1395.
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