2018
DOI: 10.1172/jci91814
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Abstract: Autophagy is important for liver homeostasis, and the deficiency leads to injury, inflammation, ductular reaction (DR), fibrosis, and tumorigenesis. It is not clear how these events are mechanistically linked to autophagy deficiency. Here, we reveal the role of high-mobility group box 1 (HMGB1) in two of these processes. First, HMGB1 was required for DR, which represents the expansion of hepatic progenitor cells (HPCs) implicated in liver repair and regeneration. DR caused by hepatotoxic diets (3,5-diethoxycar… Show more

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Cited by 86 publications
(95 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 . Interestingly, deletion of NRF2 also attenuated HMGB1 release, YAP, and mTOR activation, 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: 93%
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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 . Interestingly, deletion of NRF2 also attenuated HMGB1 release, YAP, and mTOR activation, 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: 93%
“…As discussed earlier, recent studies have revealed important roles of YAP and HMGB1 in liver pathogenesis of autophagy‐deficient liver. 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 . L‐ATG7/YAP DKO mice showed a better improvement on hepatomegaly and tumorigenesis, but these mice still developed liver tumors when they were aged .…”
Section: Discussionmentioning
confidence: 96%
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