Evidence map›Paper›PMID 40224548›Full record

ArticleBrain circulation

Protective effects of hypoxic conditioning treatment on brain and cardiac tissues following thoracic aorta occlusion.

Jun Xu, Fang Tong, Yumeng Wang, Sijie Li, Wenbo Zhao, Xiaomei Tian, Fengyong Liu, Xunming Ji, Changhong Ren

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

9 authors.

Jun XuBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Fang TongBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Yumeng WangBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Sijie LiBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Wenbo ZhaoBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Xiaomei TianDepartment of Interventional Radiology, Senior Department of Oncology, Fifth Medical Center of PLA General Hospital, Beijing, China.
Fengyong LiuDepartment of Interventional Radiology, Senior Department of Oncology, Fifth Medical Center of PLA General Hospital, Beijing, China.
Xunming JiBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Changhong RenBeijing Key Laboratory of Hypoxia Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThoracic aortic ischemia-reperfusion (I/R) injury occurs in clinical scenarios and can lead to damage in organs such as the spinal cord, kidneys, and intestines. Hypoxic postconditioning (HyP) has shown promise in reducing organ I/R injury, suggesting its potential applicability in thoracic aortic I/R injury. However, the pathological damage caused by thoracic aorta occlusion (TAO) to the heart and brain is not yet well understood. This study aims to investigate the protective effects of hypoxic conditioning (HyP) treatment on brain and cardiac tissues following TAO-induced I/R injury. MATERIALS AND

methodsMale C57BL/6 mice were used to construct the TAO model by blocking the thoracic aorta for 0.5 or 1 h, followed by 24 h of reperfusion. The mice were divided into five groups: sham, TAO (0.5 h), TAO (0.5 h) +HyP, TAO (1 h), and TAO (1 h) +HyP. Hematoxylin and eosin, Masson, and Sirius red staining were performed to assess morphological changes and collagen deposition in brain and heart tissues. Protein expression assays were conducted to quantify inflammation-related proteins in the serum.

resultsThe results showed that TAO caused significant neuronal damage in the hippocampal regions (CA1, CA3, and DG) and myocardial cell damage with collagen deposition. HyP treatment significantly alleviated these damages, particularly with shorter ischemic durations (0.5 h). Specifically, in cardiac tissues, HyP treatment reduced myocardial injury and collagen deposition. In addition, HyP treatment modulated systemic inflammatory responses, as evidenced by the increased expression of anti-inflammatory proteins such as interleukin 13 (IL-13) and the decreased expression of pro-inflammatory proteins such as IL-6, IL-12p70, IL-17, and tumor necrosis factor-α.

conclusionHyP treatment significantly mitigates brain and cardiac tissue damage caused by TAO, especially with shorter ischemic durations. These findings highlight the potential clinical application of HyP treatment in reducing TAO-induced tissue damage and inflammation, offering a novel therapeutic option for patients with thoracic aortic I/R injury. Future studies should further investigate the mechanisms and optimal implementation protocols of HyP treatment to maximize its clinical value.

Indexed as

Brain tissueCardiac tissueHypoxic conditioningInflammationIschemia-reperfusion injuryThoracic aorta occlusion

Identifiers

PMID40224548
PMCPMC11984824

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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.