2019
DOI: 10.1172/jci129234
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Abstract: In our published work, we reported that HMGB1 is actively released from autophagy-deficient hepatocytes via a pathway from NRF2 to inflammasomes to promote ductular reaction, hepatic progenitor cell expansion, and tumorigenesis. We based our conclusions on multiple lines of evidence. Release of HMGB1 from autophagy-deficient hepatocytes was documented by immunoblotting, immunostaining, and ELISA analysis in different age groups of autophagy-deficient mice. The release of HMGB1 through an active mechanism is su… Show more

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Cited by 33 publications
(117 citation statements)
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“…In great contrast, deletion of NRF2 completely abolished hepatomegaly, liver injury, inflammation, and liver tumorigenesis in either L-ATG5 or L-ATG7 KO mice. (10) Interestingly, deletion of NRF2 also attenuated HMGB1 release, YAP, and mTOR activation, (10)(11)(12) which places NRF2 activation as the upstream regulator of HMGB1 nuclear release, YAP, and mTOR activation. It is highly likely that the activation of antioxidant response due to the persistent activation of NRF2 plays a critical role in driving the progression of tumorigenesis by favoring the survival of cancer cells in the later stage of autophagy-deficient livers.…”
Section: Discussionmentioning
confidence: 95%
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“…In great contrast, deletion of NRF2 completely abolished hepatomegaly, liver injury, inflammation, and liver tumorigenesis in either L-ATG5 or L-ATG7 KO mice. (10) Interestingly, deletion of NRF2 also attenuated HMGB1 release, YAP, and mTOR activation, (10)(11)(12) which places NRF2 activation as the upstream regulator of HMGB1 nuclear release, YAP, and mTOR activation. It is highly likely that the activation of antioxidant response due to the persistent activation of NRF2 plays a critical role in driving the progression of tumorigenesis by favoring the survival of cancer cells in the later stage of autophagy-deficient livers.…”
Section: Discussionmentioning
confidence: 95%
“…However, deletion of HMGB1 only attenuated the ductular reaction and delayed the tumorigenesis but had no improvement on hepatomegaly, liver injury, and fibrosis in L-ATG7 KO mice. (11) L-ATG7/YAP DKO mice showed a better improvement on hepatomegaly and tumorigenesis, but these mice still developed liver tumors when they were aged. (12) The nuclear receptor CAR is also dispensable for hepatomegaly and liver tumorigenesis in L-ATG5 KO mice, as we demonstrated in the present study.…”
Section: Discussionmentioning
confidence: 98%
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