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Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Decoding cell death signals in liver inflammation.

Catherine Brenner1, Lorenzo Galluzzi, Oliver Kepp

  • 1INSERM, UMRS 769, LabEx LERMIT, F-92290 Châtenay Malabry, France.

Journal of Hepatology
|April 10, 2013
PubMed
Summary
This summary is machine-generated.

Hepatic inflammation can protect or harm the liver. Excessive inflammation triggers a cycle of liver cell death, leading to severe liver damage and disease.

Keywords:
5-lipoxygenase activating proteinAGERALOX5ANTASK1ATF6ApoptosisC/EPB homologous proteinCFLARCHOPCOX2CRTDAMPDAPK1DCCDIABLOECPEDNEGFREIF2AK3EPERERN1FFAFLAPFPR1GADD34GM-CSFGRP78GSK-3βHBVHCVHFDHMGB1HSCHSPIFNγILIL-1 receptor antagonistIL-1RAIRIRE1αJNKLPSLipotoxicityMAMPMAPKMBPMLKLMOMPNADPH oxidaseNAFLDNASHNKNONO synthaseNOSNOXNSAIDNecrosisNon-alcoholic necrosis steatohepatitisPERKPGAM5PGEPGE receptor 1, subtype EP1PINK1PKR-related ER kinasePP1PRRPTEN-induced putative kinase 1PTGER1PTPCPattern recognition receptorsRIPK1RNSROSS1PSIGLEC10SIRSSTAT3TGFβTLRTNF receptor 1TNF-related apoptosis inducing ligandTNFR1TNFαTRAILToll-like receptorTumor necrosis factor receptorUPRVDACaSMaseacidic sphingomyelinaseactivating transcription factor 6adenine nucleotide translocaseadvanced glycosylation end product-specific receptorapoptosis signal-regulating kinase 1arachidonate 5-lipoxygenasec-Jun N-terminal kinasecalreticulincaspase-8 and FADD-like apoptosis regulatorcyclooxygenase 2damage-associated molecular patterndeath-associated protein kinase 1deleted in colorectal carcinomadirect IAP-binding protein with low pIeIF2αeIF2α kinase 3eNOSendoplasmic reticulumendoplasmic reticulum to nucleus signaling 1endothelial NOSeosinophil cationic proteineosinophil peroxidaseeosinophil-derived neurotoxinepidermal growth factor receptoreukaryotic translation initiation factor 2αformyl peptide receptor 1free fatty acidglucose-regulated protein, 78kDaglycogen synthase kinase 3βgranulocyte macrophage colony stimulating factorgrowth arrest- and DNA damage-inducible gene 34heat-shock proteinhepatic stellate cellhepatitis B virushepatitis C virushigh mobility group box 1high-fat dietiNOSinducible NOSinositol-requiring enzyme 1αinterferon γinterleukinischemia/reperfusionlipopolysaccharidemajor basic proteinmicrobe-associated molecular patternmitochondrial outer membrane permeabilizationmitochondrial transmembrane potentialmitogen-activated protein kinasemixed lineage kinase domain-likenatural killernitric oxidenon-alcoholic fatty liver diseasenon-alcoholic steatohepatitisnon-steroidal anti-inflammatory drugpattern recognition receptorpermeability transition pore complexphosphoglycerate mutase family member 5prostaglandin Eprotein phosphatase 1reactive nitrogen speciesreactive oxygen speciesreceptor-interacting protein kinase 1sialic acid-binding Ig-like lectin 10signal transducer and activator of transcription 3sphingosine-1-phosphatesystemic inflammatory response syndrometransforming growth factor βtumor necrosis factor αunfolded protein responsevoltage-dependent anion channelΔψ(m)

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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Area of Science:

  • Hepatology
  • Immunology
  • Cellular Biology

Background:

  • Inflammation's role in liver health is complex, with mild responses aiding repair and excessive inflammation causing significant damage.
  • Conditions like fatty liver disease, hepatitis, and liver injury are exacerbated by uncontrolled hepatic inflammation.
  • Liver cells and immune cells release signals that promote hepatocyte death, creating a harmful inflammatory cycle.

Purpose of the Study:

  • To review the cellular and molecular mechanisms underlying the detrimental effects of hepatic inflammation.
  • To elucidate how inflammation initiates massive hepatocyte cell death.
  • To understand the mechanisms contributing to liver damage and disease progression.

Main Methods:

  • Review of existing literature on hepatic inflammation and cell death.
  • Analysis of cellular and molecular pathways involved in inflammatory responses in the liver.
  • Discussion of the interplay between immune cells, liver cells, and inflammatory mediators.

Main Results:

  • Mild inflammation promotes liver repair and homeostasis.
  • Excessive inflammation leads to hepatocyte apoptosis and necrosis.
  • A positive feedback loop between dying hepatocytes and immune cells amplifies liver injury.

Conclusions:

  • Hepatic inflammation is a double-edged sword, with excessive inflammation being a key driver of liver pathology.
  • Understanding these mechanisms is crucial for developing therapies for liver diseases.
  • Targeting inflammatory pathways could mitigate liver damage and prevent fibrosis and carcinogenesis.