Evidence map›Paper›PMID 26339340›Full record

ArticleInternational journal of clinical and experimental pathology2015

Bone marrow mesenchymal stem cells protect against bleomycin-induced pulmonary fibrosis in rat by activating Nrf2 signaling.

Shirong Ni, Dexuan Wang, Xiaoxiao Qiu, Lingxia Pang, Zhangjuan Song, Kunyuan Guo

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 44 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

6 authors at 2 institutions in 1 country.

Shirong NiDepartment of Hematology, Zhujiang Hospital, Southern Medical University Guangzhou, China ; Department of Pathophysiology, Wenzhou Medical University Wenzhou, Zhejiang Province, China.
Dexuan WangDepartment of Pediatrics, The Second Affiliated & Yuying Children's Hospital of Wenzhou Medical University Wenzhou, Zhejiang Province, China.
Xiaoxiao QiuDepartment of Pathophysiology, Wenzhou Medical University Wenzhou, Zhejiang Province, China.
Lingxia PangTeaching Center of Medical Functional Experiment, Wenzhou Medical University Wenzhou, Zhejiang Province, China.
Zhangjuan SongDepartment of Pathophysiology, Wenzhou Medical University Wenzhou, Zhejiang Province, China.
Kunyuan GuoDepartment of Hematology, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Wenzhou Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is a progressive and lethal disorder. Although the precise mechanisms of pulmonary fibrosis are not fully understood, oxidant/antioxidant may play an important role in many of the processes of inflammation and fibrosis. Keap1-Nrf2-ARE pathway represents one of the most important cellular defense mechanisms against oxidative stress. Mesenchymal stem cells (MSC) are in clinical trials for widespread indications including musculoskeletal, neurological, cardiac and haematological disorders. One emerging concept is that MSCs may have paracrine, rather than a functional, roles in lung injury repair and regeneration. In the present study, we investigated bone marrow mesenchymal stem cells (BMSCs) for the treatment of bleomycin-induced pulmonary fibrosis. Our results showed that BMSCs administration significantly ameliorated the bleomycin mediated histological alterations and blocked collagen deposition with parallel reduction in the hydroxyproline level. The gene expression levels of NAD(P)H: quinine oxidoreductase 1 (NQO1), gama-glutamylcysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2), attenuated by bleomycin, were increased up to basal levels after BMSCs transplantation. BMSCs significantly increased superoxide dismutase (SOD) activity and inhibited malondialdehyde (MDA) production in the injured lung. The present study provides evidence that BMSCs may be a potential therapeutic reagent for the treatment of lung fibrosis.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsBleomycinBone Marrow CellsCollagenHumansHydroxyprolineLungMalondialdehydeNF-E2-Related Factor 2Oxidative StressProtective AgentsPulmonary FibrosisRatsBleomycinCollagenHydroxyprolineMalondialdehydeNF-E2-Related Factor 2Protective Agentsantioxidant enzymesBMSCsNrf2oxidative stressPulmonary fibrosis

Identifiers

PMID26339340
PMCPMC4555668
OpenAlexW1417408206

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.