Evidence map›Paper›PMID 29445095›Full record

ArticleCell death & disease2018

Granzyme B deficiency promotes osteoblastic differentiation and calcification of vascular smooth muscle cells in hypoxic pulmonary hypertension.

Min Mao, Min Zhang, Anqi Ge, Xin Ge, Rui Gu, Chen Zhang, Yao Fu, Jiayin Gao, Xiaoying Wang, Yang Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

11 authors at 1 institution in 1 country.

Min MaoDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Min ZhangDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Anqi GeDepartment of Epidemiology, School of Public Health, Harbin Medical University, Harbin, 150081, China.
Xin GeDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Rui GuDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Chen ZhangDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Yao FuDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Jiayin GaoDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiaoying WangDepartment of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, 150081, Heilongjiang Province, China.
Yang LiuDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China.
Daling ZhuDepartment of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University (Daqing), Daqing, 163319, China. dalingz@yahoo.com.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcification is a major risk factor for vascular integrity. This pathological symptom and the underlying mechanisms in hypoxic pulmonary artery hypertension remain elusive. Here we report that pulmonary vascular medial calcification is elevated in pulmonary artery hypertension models as a result of an osteoblastic phenotype change of pulmonary arterial smooth muscle cells induced by hypoxia. Notably, inhibiting store-operated calcium channels significantly decreased osteoblastic differentiation and calcification of pulmonary arterial smooth muscle cells under hypoxia. We identified granzyme B, a major constituent of cytotoxic T lymphocytes/natural killer cell granules involved in apoptosis, as the main regulator of pulmonary arterial calcification. Overexpression of granzyme B blocked the mineralization through its effect on store-operated calcium channels in cultured pulmonary arterial smooth muscle cells under hypoxic conditions. Mice with overexpression of granzyme B exposed to hypoxia for 3 weeks showed attenuated vascular calcification and pathological progression of hypoxic pulmonary arterial hypertension. Our findings emphasize the central function of granzyme B in coordinating vascular calcification in hypoxic pulmonary arterial hypertension.

Indexed as

AnimalsApoptosisCalcinosisCalcium ChannelsCell DifferentiationGene Expression RegulationGranzymesHypertension, PulmonaryHypoxiaKiller Cells, NaturalMaleMiceMice, Inbred C57BLMice, TransgenicMonocrotalineMuscle, Smooth, VascularCalcium ChannelsGranzymesMonocrotaline

Identifiers

PMID29445095
PMCPMC5833422
OpenAlexW2792515052

What OpenQuestion holds

Textmetadata
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.