HMGB1-mediated apoptosis and autophagy in ischemic heart diseases
نویسندگان
چکیده
منابع مشابه
p53/HMGB1 complexes regulate autophagy and apoptosis.
The balance between apoptosis ("programmed cell death") and autophagy ("programmed cell survival") is important in tumor development and response to therapy. Here, we show that high mobility group box 1 (HMGB1) and p53 form a complex that regulates the balance between tumor cell death and survival. We show that knockout of p53 in HCT116 cells increases expression of cytosolic HMGB1 and induces ...
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Autophagy is a cell survival mechanism that involves degradation and recycling of cytoplasmic components, such as long-lived proteins and organelles. In addition, autophagy mediates cell death under specific circumstances. Apoptosis, a form of programmed cell death, has been well characterized, and the molecular events involved in apoptotic death are well understood. Damaged cardiomyocytes that...
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High-mobility group box 1 (HMGB1) has been found to mediate autophagy during chemotherapy in several cancers. However, whether HMGB1plays a role in autophagy and chemoresistance in bladder cancer is elusive. In this report, HMGB1 expression was found to be increased in 30 primary bladder cancer tissue specimens compared to their matched adjacent non-tumor tissues. While gemcitabine induced apop...
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The intracellular protein HMGB1 is released from cells and acts as a damage-associated molecular pattern molecule during many diseases, including inflammatory bowel disease (IBD); however, the intracellular function of HMGB1 during inflammation is poorly understood. Here, we demonstrated that cytosolic HMGB1 regulates apoptosis by protecting the autophagy proteins beclin 1 and ATG5 from calpain...
متن کاملPressure Overload Promotes HMGB1 Signaling in the Ischemic-reperfused Heart
Damage-Associated Molecular Patterns (DAMPs) are released following tissue injury and can activate proinflammatory pathways. Prototypical DAMPs include the High-Mobility Group Box 1 (HMGB1) protein which is released from necrotic cells. In turn, HMGB1 promotes inflammation via mechanisms likely involving phosphorylation/ activation of c-Jun-NH2-Terminal Kinase (JNK) and production of the inflam...
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ژورنال
عنوان ژورنال: Vascular Biology
سال: 2019
ISSN: 2516-5658
DOI: 10.1530/vb-19-0013