Evidence map›Paper›PMID 38630134›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

PLD2 deletion ameliorates sepsis-induced cardiomyopathy by suppressing cardiomyocyte pyroptosis via the NLRP3/caspase 1/GSDMD pathway.

Jun Li, Da Teng, Wenjuan Jia, Lei Gong, Haibin Dong, Chunxiao Wang, Lihui Zhang, Bowen Xu, Wenlong Wang, Lin Zhong and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. p16Journal of cardiovascular translational research · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
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

12 authors at 2 institutions in 1 country.

Jun LiSchool of Basic Medical Sciences, Qingdao University, No. 308 Ningxia Road, Qingdao, 266071, Shandong, China.
Da TengDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Wenjuan JiaDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Lei GongDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Haibin DongDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Chunxiao WangDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Lihui ZhangDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Bowen XuDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Wenlong WangDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China.
Lin ZhongDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China. yizun1971@126.com.
Jianxun WangSchool of Basic Medical Sciences, Qingdao University, No. 308 Ningxia Road, Qingdao, 266071, Shandong, China. wangjx@qdu.edu.cn.
Jun YangDepartment of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 Yudong Road, Yantai, 264000, Shandong, China. yangjyhd@163.com.
Qingdao University · CNYuhuangding Hospital · CN

Funding

National Natural Science Foundation of Shandong Province ZR2022MH151Yantai Science and Technology Innovation Development Program 2023YD037
6 · The paper itself

Abstract

objectiveSepsis-induced cardiomyopathy (SICM) is a life-threatening complication. Phospholipase D2 (PLD2) is crucial in mediating inflammatory reactions and is associated with the prognosis of patients with sepsis. Whether PLD2 is involved in the pathophysiology of SICM remains unknown. This study aimed to investigate the effect of PLD2 knockout on SICM and to explore potential mechanisms.

methodsThe SICM model was established using cecal ligation and puncture in wild-type and PLD2-knockout mice and lipopolysaccharide (LPS)-induced H9C2 cardiomyocytes. Transfection with PLD2-shRNA lentivirus and a PLD2 overexpression plasmid were used to interfere with PLD2 expression in H9C2 cells. Cardiac pathological alterations, cardiac function, markers of myocardial injury, and inflammatory factors were used to evaluate the SICM model. The expression of pyroptosis-related proteins (NLRP3, cleaved caspase 1, and GSDMD-N) was assessed using western blotting, immunofluorescence, and immunohistochemistry.

resultsSICM mice had myocardial tissue damage, increased inflammatory response, and impaired heart function, accompanied by elevated PLD2 expression. PLD2 deletion improved cardiac histological changes, mitigated cTNI production, and enhanced the survival of the SICM mice. Compared with controls, PLD2-knockdown H9C2 exhibits a decrease in inflammatory markers and lactate dehydrogenase production, and scanning electron microscopy results suggest that pyroptosis may be involved. The overexpression of PLD2 increased the expression of NLRP3 in cardiomyocytes. In addition, PLD2 deletion decreased the expression of pyroptosis-related proteins in SICM mice and LPS-induced H9C2 cells.

conclusionPLD2 deletion is involved in SICM pathogenesis and is associated with the inhibition of the myocardial inflammatory response and pyroptosis through the NLRP3/caspase 1/GSDMD pathway.

Indexed as

CardiomyopathiesCaspase 1Mice, KnockoutMyocytes, CardiacNLR Family, Pyrin Domain-Containing 3 ProteinPhospholipase DPyroptosisSepsisAnimalsCell LineGasderminsHistone-Lysine N-MethyltransferaseIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMaleMiceCasp1 protein, mouseCaspase 1GasderminsGsdmd protein, mouseHistone-Lysine N-MethyltransferaseIntracellular Signaling Peptides and ProteinsKmt2d protein, mouseLipopolysaccharidesMyeloid-Lymphoid Leukemia ProteinNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePhosphate-Binding ProteinsPhospholipase Dphospholipase D2Caspase 1GSDMDNLRP3Phospholipase D2PyroptosisSepsis-induced cardiomyopathy

Identifiers

PMID38630134
PMCPMC11106193
OpenAlexW4394873486

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.