Evidence map›Paper›PMID 26399448›Full record

ArticleAging2015

Cellular senescence-like features of lung fibroblasts derived from idiopathic pulmonary fibrosis patients.

Hagai Yanai, Albert Shteinberg, Ziv Porat, Arie Budovsky, Alex Braiman, Rolf Zeische, Vadim E Fraifeld

Erratum issuedOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 199 citations in OpenAlex.

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  14. The complexities of cell death mechanisms: a new perspective in systemic sclerosis therapy.Apoptosis : an international journal on programmed cell death · 2025
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52 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
    Zeische, Rolf [corrected to Ziesche, Rolf]
5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Hagai YanaiThe Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel.
Albert ShteinbergThe Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel.
Ziv PoratFlow Cytometry Unit, Department of Biological services, Weizmann Institute of Science, Rehovot 76100, Israel.
Arie BudovskyThe Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel.
Alex BraimanThe Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel.
Rolf ZeischeDivision of Pulmonary Medicine, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
Vadim E FraifeldThe Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel.
Ben-Gurion University of the Negev · ILCarmel (Israel) · ILMedical University of Vienna · ATWeizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is an age-related fatal disease with unknown etiology and no effective treatment. In this study, we show that primary cultures of fibroblasts derived from lung biopsies of IPF patients exhibited (i) accelerated replicative cellular senescence (CS); (ii) high resistance to oxidative-stress-induced cytotoxicity or CS; (iii) a CS-like morphology (even at the proliferative phase); and (iv) rapid accumulation of senescent cells expressing the myofibroblast marker α-SMA. Our findings suggest that CS could serve as a bridge connecting lung aging and its quite frequent outcome -- pulmonary fibrosis, and be an important player in the disease progression. Consequently, targeting senescent cells offers the potential of being a promising therapeutic approach.

Indexed as

Cellular SenescenceActinsAgedbeta-GalactosidaseCell DivisionCell ProliferationCells, CulturedCell SurvivalDisease ProgressionFibroblastsHumansLungMiddle AgedOxidative StressPulmonary FibrosisACTA2 protein, humanActinsbeta-Galactosidaseagingcellular senescencefibroblastsidiopathic pulmonary fibrosismyofibroblasts

Identifiers

PMID26399448
PMCPMC4600624
OpenAlexW2315112585

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.