It's All in the PAN: Crosstalk, Plasticity, Redundancies, Switches, and Interconnectedness Encompassed by PANoptosis Underlying the Totality of Cell Death-Associated Biological Effects.
AIM2
ASC
IRF1
MLKL
NLR
NLRP3
PANoptosis
PANoptosome
Pyrin
RIPK1
RIPK3
ZBP1
apoptosis
caspase
caspase-1
caspase-3
caspase-7
caspase-8
crosstalk
infection
inflammasome
inflammation
inflammatory cell death
innate immunity
necroptosis
plasticity
pyroptosis
redundancy
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
29 04 2022
29 04 2022
Historique:
received:
23
03
2022
revised:
23
04
2022
accepted:
23
04
2022
entrez:
14
5
2022
pubmed:
15
5
2022
medline:
18
5
2022
Statut:
epublish
Résumé
The innate immune system provides the first line of defense against cellular perturbations. Innate immune activation elicits inflammatory programmed cell death in response to microbial infections or alterations in cellular homeostasis. Among the most well-characterized programmed cell death pathways are pyroptosis, apoptosis, and necroptosis. While these pathways have historically been defined as segregated and independent processes, mounting evidence shows significant crosstalk among them. These molecular interactions have been described as 'crosstalk', 'plasticity', 'redundancies', 'molecular switches', and more. Here, we discuss the key components of cell death pathways and note several examples of crosstalk. We then explain how the diverse descriptions of crosstalk throughout the literature can be interpreted through the lens of an integrated inflammatory cell death concept, PANoptosis. The totality of biological effects in PANoptosis cannot be individually accounted for by pyroptosis, apoptosis, or necroptosis alone. We also discuss PANoptosomes, which are multifaceted macromolecular complexes that regulate PANoptosis. We consider the evidence for PANoptosis, which has been mechanistically characterized during influenza A virus, herpes simplex virus 1,
Identifiants
pubmed: 35563804
pii: cells11091495
doi: 10.3390/cells11091495
pmc: PMC9105755
pii:
doi:
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : R35 CA253095
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI101935
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI124346
Pays : United States
Organisme : NIAID NIH HHS
ID : R37 AI101935
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI160179
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR056296
Pays : United States
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