Evidence map›Paper›PMID 30533170›Full record

ArticleOxidative medicine and cellular longevity2018

Nicotine and Cotinine Inhibit Catalase and Glutathione Reductase Activity Contributing to the Impaired Osteogenesis of SCP-1 Cells Exposed to Cigarette Smoke.

Romina H Aspera-Werz, Sabrina Ehnert, Daniel Heid, Sheng Zhu, Tao Chen, Bianca Braun, Vrinda Sreekumar, Christian Arnscheidt, Andreas K Nussler

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

52 citing papers in PubMed, 85 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

9 authors at 1 institution in 1 country.

Romina H Aspera-WerzDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0002-5160-2111
Sabrina EhnertDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0003-4347-1702
Daniel HeidDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0002-1613-413X
Sheng ZhuDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0001-7078-4371
Tao ChenDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0002-1156-2899
Bianca BraunDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0003-0548-2021
Vrinda SreekumarDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.
Christian ArnscheidtDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.
Andreas K NusslerDepartment of Traumatology, University of Tübingen, Schnarrenbergstraße 95, 72076 Tübingen, Germany.ORCID 0000-0002-6666-6791
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking has been identified as a major risk factor for osteoporosis decades ago. Several studies have shown a direct relationship between cigarette smoking, decreased bone mineral density, and impaired fracture healing. However, the mechanisms behind impaired fracture healing and cigarette smoking are yet to be elucidated. Migration and osteogenesis of mesenchymal stem/stromal cells (MSCs) into the fracture site play a vital role in the process of fracture healing. In human nicotine, the most pharmacologically active and major addictive component present in tobacco gets rapidly metabolized to the more stable cotinine. This study demonstrates that physiological concentrations of both nicotine and cotinine do not affect the osteogenic differentiation of MSCs. However, cigarette smoke exposure induces oxidative stress by increasing superoxide radicals and reducing intracellular glutathione in MSCs, negatively affecting osteogenic differentiation. Although, not actively producing reactive oxygen species (ROS) nicotine and cotinine inhibit catalase and glutathione reductase activity, contributing to an accumulation of ROS by cigarette smoke exposure. Coincubation with N-acetylcysteine or L-ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in smokers.

Indexed as

AntioxidantsCatalaseCell DifferentiationCell LineCotinineGlutathione ReductaseHumansMesenchymal Stem CellsNicotineOsteogenesisReactive Oxygen SpeciesSmokeTobacco ProductsAntioxidantsCatalaseCotinineGlutathione ReductaseNicotineReactive Oxygen SpeciesSmoke

Identifiers

PMID30533170
PMCPMC6250005
OpenAlexW2899604438

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.