Evidence map›Paper›PMID 39825405›Full record

ArticleJournal of translational medicine2025

Parthenolide improves sepsis-induced coagulopathy by inhibiting mitochondrial-mediated apoptosis in vascular endothelial cells through BRD4/BCL-xL pathway.

Jun Zhang, Xing Zhu, Yong Li, Yinyu Wu, Yunxia Du, Hai Yang, Zhengchao Liu, Haoyu Pei, Rui Li, Huan Luo and 3 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Protective effects ofFrontiers in nutrition · 2025
    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

13 authors.

Jun Zhang *Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Xing Zhu *Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Yong Li *Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Yinyu WuDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Yunxia DuDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Hai YangDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Zhengchao LiuDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Haoyu PeiDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Rui LiDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Huan LuoDepartment of Critical Care Medicine, Chongqing General Hospital, Chongqing University, Chongqing, 401147, China.
Deyu ZuoDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Chongqing University of Chinese Medicine, Chongqing Traditional Chinese Medicine Hospital, No.6, Panxi 7Th Branch Road, Jiangbei District, Chongqing, 400021, China. zuodeyu@cqctcm.edu.cn.
Han SheDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China. sh1990@tmmu.edu.cn.
Qingxiang MaoDepartment of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China. qxmao@tmmu.edu.cn.

Funding

the Chongqing Medical Young Talents Program YXQN202415the Chongqing Medical Young Talents Program YXQN202452the Chongqing Natural Science Foundation Innovation and Development Joint Fund (Chongqing Education Commission) CSTB2024NSCQ- LZX0079the Chongqing Talent Program: Innovative leading talents CSTC2024YCJH-BGZXM0011the National Natural Science Foundation of China 82300561the National Natural Science Foundation of China 82305006the Natural Science Foundation of Chongqing CSTB2022NSCQ-MSX0174the Natural Science Foundation of Chongqing CSTB2023NSCQ-MSX0713the Youth Program of Joint Medical Research of Chongqing Science and Chongqing Health Commission 2025QNXM038
6 · The paper itself

Abstract

backgroundSepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear.

methodsThe study utilized septic rats and lipopolysaccharide (LPS)-stimulated VECs to simulate a SIC model and observe the therapeutic effects of PTL. Additionally, nanotechnology was employed to produce Nano-PTL (N-PTL), to observe whether it has advantages over PTL in treating SIC.

resultsPTL has been shown to mitigate lung injury in septic rats, significantly reduce tumor necrosis factor-α (TNF-α) levels, and increase survival rates. PTL treatment also enhances coagulation function, augments vascular endothelial cell (VEC) function, reduces mitochondrial fragmentation, and increases both mitochondrial oxygen consumption rate (OCR) and mitochondrial membrane potential (MMP), while inhibiting reactive oxygen species (ROS) production. By increasing BRD4/BCL-xL levels, PTL can prevent mitochondrial-mediated apoptosis in VECs, improve VEC function, and consequently ameliorate SIC. Additionally, nanotechnology-synthesized N-PTL further enhances the protective effects on VECs and coagulation function.

conclusionsThis study clarifies the therapeutic effects and mechanisms of PTL on SIC, offering new strategies and directions for the treatment of sepsis.

Indexed as

ApoptosisBlood Coagulation DisordersEndothelial CellsMitochondriaSepsisSesquiterpenesSignal TransductionTranscription FactorsAnimalsCell Cycle ProteinsHumansLipopolysaccharidesMaleMembrane Potential, MitochondrialRatsRats, Sprague-DawleyCell Cycle ProteinsLipopolysaccharidesparthenolideReactive Oxygen SpeciesSesquiterpenesTranscription FactorsApoptosisMitochondriaParthenolideSepsis-induced coagulopathyVascular endothelial cells

Identifiers

PMID39825405
PMCPMC11740428

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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.