Pyroptosis is a critical immune-inflammatory response involved in atherosclerosis

[Display omitted] Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lip...

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Published inPharmacological research Vol. 165; p. 105447
Main Authors He, Xiao, Fan, Xuehui, Bai, Bing, Lu, Nanjuan, Zhang, Shuang, Zhang, Liming
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.03.2021
Subjects
Animals
Atherosclerosis
Atherosclerosis - immunology
Atherosclerosis - metabolism
Cholesterol crystals
Endothelial Cells - immunology
Endothelial Cells - metabolism
Humans
Immunity, Cellular - immunology
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
Lipoproteins, LDL - immunology
Lipoproteins, LDL - metabolism
Macrophages - immunology
Macrophages - metabolism
Myocytes, Smooth Muscle - immunology
Myocytes, Smooth Muscle - metabolism
ox-LDL
Pyroptosis
Pyroptosis - immunology
NADPH
DY9836 (PubChem CID:9801925)
COX-2
MCC950 (PubChem CID: 9910393)
mtDNA
Leu-Leu-OMe (PubChem CID:7016877)
4-PBA (PubChem CID:83242)
ICAM-1
HO-1
HMGB1
cAMP
INF39 (PubChem CID: 69150705)
DAMPs
LDH
Cholesterol crystals
UPR
CA-074-Me (PubChem CID:6610318)
Atherosclerosis
BKCa
PAMPs
CHOP
mtROS
mTOP
z-VAD-fmk (PubChem CID:87146076)
ASCs
AMI
VX-765 (PubChem CID:11398092)
GSDMD
XBP1
Pyroptosis
MMPs
Taurine (PubChem CID:1123)
TET2
CHCs
ox-LDL
ER
VCAM-1
NOX
ROS
VDAC
TXNIP
SiNPs
MAMs
m6A
MALAT1
TLRs
BMS-345541 (PubChem CID:9926054)
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Abstract [Display omitted] Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lipoprotein (ox-LDL) and cholesterol crystals, have been shown to promote pyroptosis through several mechanisms that involve ion flux, ROS, endoplasmic reticulum stress, mitochondrial dysfunction, lysosomal rupture, Golgi function, autophagy, noncoding RNAs, post-translational modifications, and the expression of related molecules. Pyroptosis of endothelial cells, macrophages, and smooth muscle cells in the vascular wall can induce plaque instability and accelerate atherosclerosis progression. In this review, we focus on the pathogenesis, influence, and therapy of pyroptosis in atherosclerosis and provide novel ideas for suppressing pyroptosis and the progression of atherosclerosis.
AbstractList Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lipoprotein (ox-LDL) and cholesterol crystals, have been shown to promote pyroptosis through several mechanisms that involve ion flux, ROS, endoplasmic reticulum stress, mitochondrial dysfunction, lysosomal rupture, Golgi function, autophagy, noncoding RNAs, post-translational modifications, and the expression of related molecules. Pyroptosis of endothelial cells, macrophages, and smooth muscle cells in the vascular wall can induce plaque instability and accelerate atherosclerosis progression. In this review, we focus on the pathogenesis, influence, and therapy of pyroptosis in atherosclerosis and provide novel ideas for suppressing pyroptosis and the progression of atherosclerosis.Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lipoprotein (ox-LDL) and cholesterol crystals, have been shown to promote pyroptosis through several mechanisms that involve ion flux, ROS, endoplasmic reticulum stress, mitochondrial dysfunction, lysosomal rupture, Golgi function, autophagy, noncoding RNAs, post-translational modifications, and the expression of related molecules. Pyroptosis of endothelial cells, macrophages, and smooth muscle cells in the vascular wall can induce plaque instability and accelerate atherosclerosis progression. In this review, we focus on the pathogenesis, influence, and therapy of pyroptosis in atherosclerosis and provide novel ideas for suppressing pyroptosis and the progression of atherosclerosis.
[Display omitted] Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lipoprotein (ox-LDL) and cholesterol crystals, have been shown to promote pyroptosis through several mechanisms that involve ion flux, ROS, endoplasmic reticulum stress, mitochondrial dysfunction, lysosomal rupture, Golgi function, autophagy, noncoding RNAs, post-translational modifications, and the expression of related molecules. Pyroptosis of endothelial cells, macrophages, and smooth muscle cells in the vascular wall can induce plaque instability and accelerate atherosclerosis progression. In this review, we focus on the pathogenesis, influence, and therapy of pyroptosis in atherosclerosis and provide novel ideas for suppressing pyroptosis and the progression of atherosclerosis.
Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the secretion of inflammatory cytokines (IL-1β and IL-18). Atherosclerosis-related risk factors, including oxidized low-density lipoprotein (ox-LDL) and cholesterol crystals, have been shown to promote pyroptosis through several mechanisms that involve ion flux, ROS, endoplasmic reticulum stress, mitochondrial dysfunction, lysosomal rupture, Golgi function, autophagy, noncoding RNAs, post-translational modifications, and the expression of related molecules. Pyroptosis of endothelial cells, macrophages, and smooth muscle cells in the vascular wall can induce plaque instability and accelerate atherosclerosis progression. In this review, we focus on the pathogenesis, influence, and therapy of pyroptosis in atherosclerosis and provide novel ideas for suppressing pyroptosis and the progression of atherosclerosis.
ArticleNumber 105447
Author Fan, Xuehui
Bai, Bing
Zhang, Shuang
Zhang, Liming
He, Xiao
Lu, Nanjuan
Author_xml – sequence: 1
  givenname: Xiao
  orcidid: 0000-0003-4214-0389
  surname: He
  fullname: He, Xiao
  email: hexiao1992prime@163.com
  organization: Department of Neurology, First Affiliated Hospital of Harbin Medical University, 23 You Zheng Street, Harbin 150001, Heilongjiang Province, China
– sequence: 2
  givenname: Xuehui
  orcidid: 0000-0002-5592-1750
  surname: Fan
  fullname: Fan, Xuehui
  email: fanxuehui1993@126.com
  organization: Department of Neurology, First Affiliated Hospital of Harbin Medical University, 23 You Zheng Street, Harbin 150001, Heilongjiang Province, China
– sequence: 3
  givenname: Bing
  orcidid: 0000-0002-1306-5343
  surname: Bai
  fullname: Bai, Bing
  email: bingbai1224@outlook.com
  organization: Department of Neurology, First Affiliated Hospital of Harbin Medical University, 23 You Zheng Street, Harbin 150001, Heilongjiang Province, China
– sequence: 4
  givenname: Nanjuan
  surname: Lu
  fullname: Lu, Nanjuan
  email: lunanjuan20@163.com
  organization: Department of Neurology, First Affiliated Hospital of Harbin Medical University, 23 You Zheng Street, Harbin 150001, Heilongjiang Province, China
– sequence: 5
  givenname: Shuang
  orcidid: 0000-0003-2189-865X
  surname: Zhang
  fullname: Zhang, Shuang
  email: 1663989328@qq.com
  organization: General Surgery, Harbin Changzheng Hospital, 363 Xuan Hua Street, Harbin 150001, Heilongjiang Province, China
– sequence: 6
  givenname: Liming
  orcidid: 0000-0003-2255-0030
  surname: Zhang
  fullname: Zhang, Liming
  email: vic_hx@163.com
  organization: Department of Neurology, First Affiliated Hospital of Harbin Medical University, 23 You Zheng Street, Harbin 150001, Heilongjiang Province, China
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ID FETCH-LOGICAL-c422t-bf587841c986c1e4e0c9c5bdda7162a12e92fdaf8ff76a8f23d7123c2fd30f3c3
IEDL.DBID .~1
ISSN 1043-6618
1096-1186
IngestDate Fri Jul 11 13:06:58 EDT 2025
Wed Feb 19 02:27:14 EST 2025
Tue Jul 01 03:33:48 EDT 2025
Thu Apr 24 22:55:58 EDT 2025
Fri Feb 23 02:40:53 EST 2024
IsPeerReviewed true
IsScholarly true
Keywords NADPH
DY9836 (PubChem CID:9801925)
COX-2
MCC950 (PubChem CID: 9910393)
mtDNA
Leu-Leu-OMe (PubChem CID:7016877)
4-PBA (PubChem CID:83242)
ICAM-1
HO-1
HMGB1
cAMP
INF39 (PubChem CID: 69150705)
DAMPs
LDH
Cholesterol crystals
UPR
CA-074-Me (PubChem CID:6610318)
Atherosclerosis
BKCa
PAMPs
CHOP
mtROS
mTOP
z-VAD-fmk (PubChem CID:87146076)
ASCs
AMI
VX-765 (PubChem CID:11398092)
GSDMD
XBP1
Pyroptosis
MMPs
Taurine (PubChem CID:1123)
TET2
CHCs
ox-LDL
ER
VCAM-1
NOX
ROS
VDAC
TXNIP
SiNPs
MAMs
m6A
MALAT1
TLRs
BMS-345541 (PubChem CID:9926054)
Language English
License Copyright © 2021 Elsevier Ltd. All rights reserved.
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MergedId FETCHMERGED-LOGICAL-c422t-bf587841c986c1e4e0c9c5bdda7162a12e92fdaf8ff76a8f23d7123c2fd30f3c3
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content type line 23
ORCID 0000-0002-1306-5343
0000-0002-5592-1750
0000-0003-2255-0030
0000-0003-4214-0389
0000-0003-2189-865X
PMID 33516832
PQID 2484161569
PQPubID 23479
ParticipantIDs proquest_miscellaneous_2484161569
pubmed_primary_33516832
crossref_citationtrail_10_1016_j_phrs_2021_105447
crossref_primary_10_1016_j_phrs_2021_105447
elsevier_sciencedirect_doi_10_1016_j_phrs_2021_105447
ProviderPackageCode CITATION
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PublicationDate March 2021
2021-03-00
20210301
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PublicationDate_xml – month: 03
  year: 2021
  text: March 2021
PublicationDecade 2020
PublicationPlace Netherlands
PublicationPlace_xml – name: Netherlands
PublicationTitle Pharmacological research
PublicationTitleAlternate Pharmacol Res
PublicationYear 2021
Publisher Elsevier Ltd
Publisher_xml – name: Elsevier Ltd
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Snippet [Display omitted] Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore...
Pyroptosis is a form of programmed cell death activated by various stimuli and is characterized by inflammasome assembly, membrane pore formation, and the...
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SubjectTerms Animals
Atherosclerosis
Atherosclerosis - immunology
Atherosclerosis - metabolism
Cholesterol crystals
Endothelial Cells - immunology
Endothelial Cells - metabolism
Humans
Immunity, Cellular - immunology
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
Lipoproteins, LDL - immunology
Lipoproteins, LDL - metabolism
Macrophages - immunology
Macrophages - metabolism
Myocytes, Smooth Muscle - immunology
Myocytes, Smooth Muscle - metabolism
ox-LDL
Pyroptosis
Pyroptosis - immunology
Title Pyroptosis is a critical immune-inflammatory response involved in atherosclerosis
URI https://dx.doi.org/10.1016/j.phrs.2021.105447
https://www.ncbi.nlm.nih.gov/pubmed/33516832
https://www.proquest.com/docview/2484161569
Volume 165
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