ArticleMolecular and cellular biology2007
Bid-independent mitochondrial activation in tumor necrosis factor alpha-induced apoptosis and liver injury.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Hepatocyte Bcl-3 protects from death-receptor mediated apoptosis and subsequent acute liver failure.Cell death & disease · 2022Article
- Article
- Gasdermins in Apoptosis: New players in an Old Game.The Yale journal of biology and medicine · 2019Review
- Loss of PDK4 switches the hepatic NF-κB/TNF pathway from pro-survival to pro-apoptosis.Hepatology (Baltimore, Md.) · 2018Article
- Deficiency of pyruvate dehydrogenase kinase 4 sensitizes mouse liver to diethylnitrosamine and arsenic toxicity through inducing apoptosis.Liver research (Beijing, China) · 2018Article
- A novel scoring system based on common laboratory tests predicts the efficacy of TNF-inhibitor and IL-6 targeted therapy in patients with rheumatoid arthritis: a retrospective, multicenter observational study.Arthritis research & therapy · 2017Observational
- Caspase Inhibition Prevents Tumor Necrosis Factor-α-Induced Apoptosis and Promotes Necrotic Cell Death in Mouse Hepatocytes in Vivo and in Vitro.The American journal of pathology · 2016Article
- Protein kinase C-β inhibitor treatment attenuates hepatic ischemia and reperfusion injury in diabetic rats.Experimental and therapeutic medicine · 2016Article
- JNK1/2 regulate Bid by direct phosphorylation at Thr59 in response to ALDH1L1.Cell death & disease · 2014Article
- Rejuvenating Bi(d)ology.Oncogene · 2013Review
- Mitochondrial permeability transition in rat hepatocytes after anoxia/reoxygenation: role of Ca2+-dependent mitochondrial formation of reactive oxygen species.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Modeling the TNFα-induced apoptosis pathway in hepatocytes.PloS one · 2011Article
- Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice.The Journal of clinical investigation · 2010Article
- Deficiency of Bid protein reduces sepsis-induced apoptosis and inflammation, while improving septic survival.Shock (Augusta, Ga.) · 2010Article
- VDAC2 is required for truncated BID-induced mitochondrial apoptosis by recruiting BAK to the mitochondria.EMBO reports · 2009Article
- The strength of the Fas ligand signal determines whether hepatocytes act as type 1 or type 2 cells in murine livers.Hepatology (Baltimore, Md.) · 2009Article
- A nanoconjugate Apaf-1 inhibitor protects mesothelial cells from cytokine-induced injury.PloS one · 2009Article
- Genetic delineation of the pathways mediated by bid and JNK in tumor necrosis factor-alpha-induced liver injury in adult and embryonic mice.The Journal of biological chemistry · 2009Article
- Fatal hepatitis mediated by tumor necrosis factor TNFalpha requires caspase-8 and involves the BH3-only proteins Bid and Bim.Immunity · 2009Article
- Tumor necrosis factor-alpha induces intrinsic apoptotic signaling during renal obstruction through truncated bid activation.The Journal of urology · 2008Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The death receptor apoptosis pathway is intimately connected with the mitochondrial apoptosis pathway. Bid is a BH3-only pro-death Bcl-2 family protein and is the major molecule linking the two pathways. Bid-mediated mitochondrial activation occurs early and is responsible for the prompt progress of tumor necrosis factor alpha (TNF-alpha)-induced apoptosis. However, in both cultured cells and animal models of TNF-alpha-induced injury, later-phase Bid-independent mitochondrial activation could be demonstrated. Consequently, bid-deficient mice are still susceptible to endotoxin-induced liver injury and mortality. Notably, embryonic hepatocyte apoptosis and lethality caused by TNF-alpha in the absence of p65relA cannot be rescued by the simultaneous deletion of bid. Further studies indicate that multiple mechanisms including reactive oxygen species, JNK, and permeability transition are critically involved in Bid-independent mitochondrial activation. Inhibition of these events suppresses TNF-alpha-induced mitochondrial activation and apoptosis in bid-deficient cells. These findings thus indicate that there are at least two sets of mechanisms of mitochondrial activation upon TNF-alpha stimulation. While the Bid-mediated mechanism is rapid and potent, the Bid-independent mechanism progresses gradually and involves multiple players. The critical involvement of Bid-independent mitochondrial activation in TNF-alpha-induced apoptosis demands the intervention of TNF-alpha-mediated tissue injury via multiple avenues.
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