Evidence map›Paper›PMID 27607578›Full record

ArticleCell death & disease2016

Hemorrhagic shock primes for lung vascular endothelial cell pyroptosis: role in pulmonary inflammation following LPS.

Jie Yang, Yanfeng Zhao, Peng Zhang, Yuehua Li, Yong Yang, Yang Yang, Junjie Zhu, Xiao Song, Gening Jiang, Jie Fan

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026
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  9. Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026
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17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Jie YangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Yanfeng ZhaoDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Peng ZhangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Yuehua LiDepartment of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Yong YangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Yang YangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Junjie ZhuDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Xiao SongDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Gening JiangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Jie FanDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Tongji University · CNShanghai Pulmonary Hospital · CNUniversity of Pittsburgh · USVA Pittsburgh Healthcare System · US

Funding

Regulation of Intestinal Mucosal Injury & Repair After Trauma/Hemorrhagic ShockP50GM053789 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1997 to 2013
$18.0M
IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
Cell Priming, Receptor Cross-Talk, and Acute Lung InjuryR01HL079669 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAN, JIE, WILSON, MARK A. · 2005 to 2019
$4.0M
Aging-Related Mechanism of Post-Hemorrhagic Shock Acute Lung InjuryR56HL123882 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAN, JIE · 2015 to 2015
$385k
Cell Death Mechanism of Acute Lung Injury in SepsisI01BX002729 · VA · VETERANS HEALTH ADMINISTRATION · PI FAN, JIE · 2015 to 2020
–
BLRD VA I01 BX002729NHLBI NIH HHS R01 HL076179NHLBI NIH HHS R01 HL079669NHLBI NIH HHS R56 HL123882NIGMS NIH HHS P50 GM053789
6 · The paper itself

Abstract

Hemorrhagic shock (HS) often renders patients more susceptible to lung injury by priming for an exaggerated response to a second infectious stimulus. Acute lung injury (ALI) is a major component of multiple organ dysfunction syndrome following HS and regularly serves as a major cause of patient mortality. The lung vascular endothelium is an active organ that has a central role in the development of ALI through synthesizing and releasing of a number of inflammatory mediators. Cell pyroptosis is a caspase-1-dependent regulated cell death, which features rapid plasma membrane rupture and release of proinflammatory intracellular contents. In this study, we demonstrated an important role of HS in priming for LPS-induced lung endothelial cell (EC) pyroptosis. We showed that LPS through TLR4 activates Nlrp3 (NACHT, LRR, and PYD domains containing protein 3) inflammasome in mouse lung vascular EC, and subsequently induces caspase-1 activation. However, HS induced release of high-mobility group box 1 (HMGB1), which acting through the receptor for advanced glycation end products initiates EC endocytosis of HMGB1, and subsequently triggers a cascade of molecular events, including cathepsin B release from ruptured lysosomes followed by pyroptosome formation and caspase-1 activation. These HS-induced events enhance LPS-induced EC pyroptosis. We further showed that lung vascular EC pyroptosis significantly exaggerates lung inflammation and injury. The present study explores a novel mechanism underlying HS-primed ALI and thus presents a potential therapeutic target for post-HS ALI.

Indexed as

Acute Lung InjuryAnimalsCaspase 1Cathepsin BEndothelial CellsGene Expression RegulationHMGB1 ProteinInflammasomesLipopolysaccharidesLungLysosomesMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinPrimary Cell CultureCaspase 1Cathepsin BCtsb protein, mouseHMGB1 ProteinHMGB1 protein, mouseInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID27607578
PMCPMC5059873
OpenAlexW2510919342

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.