Evidence map›Paper›PMID 20427009›Full record

ReviewThe ocular surface2010

Mechanisms involved in injury and repair of the murine lacrimal gland: role of programmed cell death and mesenchymal stem cells.

Driss Zoukhri

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in The ocular surface, 2010. 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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Driss ZoukhriDepartment of General Dentistry, Tufts University School of Dental Medicine, Boston, MA, USA. driss.zoukhri@tufts.edu
Tufts University · US

Funding

STIMULUS/SECRETION COUPLING IN DISEASED LACRIMAL GLANDR01EY012383 · NEI · TUFTS UNIVERSITY BOSTON · PI ZOUKHRI, DRISS · 1999 to 2015
$5.2M
NEI NIH HHS R01 EY012383NEI NIH HHS R01-EY12383
6 · The paper itself

Abstract

The non-keratinized epithelia of the ocular surface are constantly challenged by environmental insults, such as smoke, dust, and airborne pathogens. Tears are the sole physical protective barrier for the ocular surface. Production of tears in inadequate quantity or of inadequate quality results in constant irritation of the ocular surface, leading to dry eye disease, also referred to as keratoconjunctivitis sicca (KCS). Inflammation of the lacrimal gland, such as occurs in Sjogren syndrome, sarcoidosis, chronic graft-versus-host disease, and other pathological conditions, results in inadequate secretion of the aqueous layer of the tear film and is a leading cause of dry eye disease. The hallmarks of lacrimal gland inflammation are the presence of immune cell infiltrates, loss of acinar epithelial cells (the secreting cells), and increased production of proinflammatory cytokines. To date, the mechanisms leading to acinar cell loss and the associated decline in lacrimal gland secretion are still poorly understood. It is also not understood why the remaining lacrimal gland cells are unable to proliferate in order to regenerate a functioning lacrimal gland. This article reviews recent advances in exocrine tissue injury and repair, with emphasis on the roles of programmed cell death and stem/progenitor cells.

Indexed as

ApoptosisAutophagyWound HealingAnimalsDacryocystitisLacrimal ApparatusMesenchymal Stem CellsMiceSjogren's Syndrome

Identifiers

PMID20427009
PMCPMC3225027
OpenAlexW2067655781

What OpenQuestion holds

Textmetadata
LicenceTDM
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.