Evidence map›Paper›PMID 28361925›Full record

ArticleScientific reports2017

Follistatin-like 1 protects against hypoxia-induced pulmonary hypertension in mice.

Wei Zhang, Wang Wang, Jie Liu, Jinna Li, Juan Wang, Yunxia Zhang, Zhifei Zhang, Yafei Liu, Yankun Jin, Jifeng Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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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

14 authors at 5 institutions in 1 country.

Wei ZhangDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Wang WangDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Jie LiuDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Jinna LiRespiratory Department, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Juan WangRespiratory Department, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Yunxia ZhangDepartment of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Zhifei ZhangDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Yafei LiuDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Yankun JinDepartment of Respiratory and Critical Care Medicine, China-Japan Friendship Hospital, Beijing 100029, P.R. China.
Jifeng LiDepartment of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Jie CaoRespiratory Department, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Chen WangBeijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Capital Medical University, Beijing 100069, P.R. China.
Wen NingState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin 300071, P.R. China.
Jun WangDepartment of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.
Capital Medical University · CNBeijing Chao-Yang Hospital · CNChina-Japan Friendship Hospital · CNNankai University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) remains a life-limiting disease characterized by pulmonary vascular remodelling due to aberrant proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), thus leading to raised pulmonary arterial pressure and right ventricular hypertrophy. Secreted glycoprotein follistatin-like 1 (FSTL1) has been reported to ameliorate tissue remodelling in cardiovascular injuries. However, the role of FSTL1 in deranged pulmonary arteries remains elusive. We found that there were higher serum levels of FSTL1 in patients with PH related to chronic obstructive pulmonary diseases (COPD) and in mice model of hypoxia-induced PH (HPH). Haploinsufficiency of Fstl1 in mice contributed to an exacerbated HPH, as demonstrated by increased right ventricular systolic pressure, pulmonary arterial muscularization and right ventricular hypertrophy index. Conversely, FSTL1 administration attenuated HPH. In cultured human PASMCs, hypoxia-promoted cellular viability, DNA synthesis and migration were suppressed by exogenous FSTL1 but enhanced by small interfering RNA targeting FSTL1. Additionally, FSTL1 inhibited the proliferation and migration of PASMCs via extracellular regulated kinase (ERK) signal pathway. All these findings indicate that FSTL1 imposed a protective modulation on pulmonary vascular remodelling, thereby suggesting its role in the regulation of HPH.

Indexed as

AnimalsCell ProliferationCells, CulturedDisease Models, AnimalFollistatin-Related ProteinsHumansHypertension, PulmonaryHypoxiaMiceMyocytes, Smooth MusclePulmonary ArteryPulmonary Disease, Chronic ObstructiveRNA, Small InterferingFollistatin-Related ProteinsFSTL1 protein, humanFstl1 protein, mouseRNA, Small Interfering

Identifiers

PMID28361925
PMCPMC5374469
OpenAlexW2597573949

What OpenQuestion holds

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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.