Evidence map›Paper›PMID 27419637›Full record

ArticleOncotarget2016

Mitochondrial transplantation attenuates hypoxic pulmonary hypertension.

Liping Zhu, Jiwei Zhang, Juan Zhou, Yankai Lu, Songling Huang, Rui Xiao, Xiangyuan Yu, Xianqin Zeng, Bingxun Liu, Fangbo Liu and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  19. Emerging roles of mitochondria in animal regeneration.Cell regeneration (London, England) · 2023
    Review
  20. Mitochondrial Transfer Regulates Cell Fate Through Metabolic Remodeling in Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    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

17 authors at 2 institutions in 1 country.

Liping ZhuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Jiwei ZhangDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Juan ZhouDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Yankai LuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Songling HuangDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Rui XiaoDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Xiangyuan YuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Xianqin ZengDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Bingxun LiuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Fangbo LiuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Mengxiang SunDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Mao DaiDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Qiang HaoDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Jiansha LiKey Laboratory of Pulmonary Diseases of Ministry of Health, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Tao WangKey Laboratory of Pulmonary Diseases of Ministry of Health, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Tongfei LiDepartment of Pathology, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, China.
Qinghua HuDepartment of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are essential for the onset of hypoxia-induced pulmonary vasoconstriction and pulmonary vascular-remodeling, two major aspects underlying the development of pulmonary hypertension, an incurable disease. However, hypoxia induces relaxation of systemic arteries such as femoral arteries and mitochondrial heterogeneity controls the distinct responses of pulmonary versus femoral artery smooth muscle cells to hypoxia in vitro. The aim of this study was to determine whether mitochondrial heterogeneity can be experimentally exploited in vivo for a potential treatment against pulmonary hypertension. The intact mitochondria were transplanted into Sprague-Dawley rat pulmonary artery smooth muscle cells in vivo via intravenous administration. The immune-florescent staining and ultrastructural examinations on pulmonary arteries confirmed the intracellular distribution of exogenous mitochondria and revealed the possible mitochondrial transfer from pulmonary artery endothelial cells into smooth muscle cells in part through their intercellular space and intercellular junctions. The transplantation of mitochondria derived from femoral artery smooth muscle cells inhibited acute hypoxia-triggered pulmonary vasoconstriction, attenuated chronic hypoxia-induced pulmonary vascular remodeling, and thus prevented the development of pulmonary hypertension or cured the established pulmonary hypertension in rats exposed to chronic hypoxia. Our findings suggest that mitochondrial transplantation possesses potential implications for exploring a novel therapeutic and preventive strategy against pulmonary hypertension.

Indexed as

Administration, IntravenousAnimalsFemoral ArteryHypertension, PulmonaryHypoxiaMitochondriaMuscle, Smooth, VascularMyocytes, Smooth MusclePulmonary ArteryRatsRats, Sprague-DawleyVasoconstrictionhypoxiamitochondriaPathology Sectionpulmonary hypertensiontransplantationvasoconstriction

Identifiers

PMID27419637
PMCPMC5226481
OpenAlexW2462913190

What OpenQuestion holds

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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 OpenQuestion graph.