Evidence map›Paper›PMID 27279915›Full record

ArticleTheranostics2016

Mitochondrial Transplantation Attenuates Airway Hyperresponsiveness by Inhibition of Cholinergic Hyperactivity.

Yuan Su, Liping Zhu, Xiangyuan Yu, Lei Cai, Yankai Lu, Jiwei Zhang, Tongfei Li, Jiansha Li, Jingyan Xia, Feng Xu and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Theranostics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Mitochondrial dysfunction: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024
    Review
  7. Review
  8. Targeted Mitochondrial Delivery to Hepatocytes: A Review.Journal of clinical and translational hepatology · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Yuan Su1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);; 2. Department of Respiratory Medicine, Union Hospital, Tongji Medical College, HUST, Wuhan 430022, PRC;
Liping Zhu1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);
Xiangyuan Yu1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);
Lei Cai1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);
Yankai Lu1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);
Jiwei Zhang1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);; 3. Department of Pathology, Union Hospital, Tongji Medical College, HUST, Wuhan 430030, PRC;
Tongfei Li4. Department of Pathology, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, PRC;
Jiansha Li1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);; 5. Department of Pathology, Tongji Hospital, Tongji Medical College, HUST, Wuhan 430030, PRC;
Jingyan Xia6. Department of Radiation Oncology, Second Affiliated Hospital, Zhejiang University School of Medicine (ZUSM), Hangzhou 310009, PRC;
Feng Xu7. Department of Infectious Diseases, Second Affiliated Hospital, ZUSM, Hangzhou 310009, PRC;
Qinghua Hu1. Key Laboratory of Pulmonary Diseases of Ministry of Health and Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan 430030, People's Republic of China (PRC);; 8. Key Laboratory of Molecular Biophysics of the Ministry of Education, HUST, PRC.
Huazhong University of Science and Technology · CNSecond Affiliated Hospital of Zhejiang University · CNHubei University of Medicine · CNMinistry of Education · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased cholinergic activity has been highlighted in the pathogenesis of airway hyperresponsiveness, and alternations of mitochondrial structure and function appear to be involved in many lung diseases including airway hyperresponsiveness. It is crucial to clarify the cause-effect association between mitochondrial dysfunction and cholinergic hyperactivity in the pathogenesis of airway hyperresponsiveness. Male SD rats and cultured airway epithelial cells were exposed to cigarette smoke plus lipopolysaccharide administration; mitochondria isolated from airway epithelium were delivered into epithelial cells in vitro and in vivo. Both the cigarette smoke plus lipopolysaccharide-induced cholinergic hyperactivity in vitro and the airway hyperresponsiveness to acetylcholine in vivo were reversed by the transplantation of exogenous mitochondria. The rescue effects of exogenous mitochondria were imitated by the elimination of excessive reactive oxygen species or blockage of muscarinic M3 receptor, but inhibited by M receptor enhancer. Mitochondrial transplantation effectively attenuates cigarette smoke plus lipopolysaccharide-stimulated airway hyperresponsiveness through the inhibition of ROS-enhanced epithelial cholinergic hyperactivity.

Indexed as

AnimalsCholinergic AgentsEpithelial CellsMaleMitochondriaNon-Neuronal Cholinergic SystemRats, Sprague-DawleyReactive Oxygen SpeciesReceptor, Muscarinic M3Respiratory HypersensitivityCholinergic AgentsReactive Oxygen SpeciesReceptor, Muscarinic M3airway hyperresponsivenesscholinergic hyperactivitymitochondrial transplantation

Identifiers

PMID27279915
PMCPMC4893649
OpenAlexW2417461411

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.