Evidence map›Paper›PMID 27207516›Full record

ArticleDiabetes2016

Mast Cells Regulate Wound Healing in Diabetes.

Ana Tellechea, Ermelindo C Leal, Antonios Kafanas, Michael E Auster, Sarada Kuchibhotla, Yana Ostrovsky, Francesco Tecilazich, Dimitrios Baltzis, Yongjun Zheng, Eugénia Carvalho and 8 more

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 169 citations in OpenAlex.

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  12. AcCells · 2025
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28 more citing papers are in PubMed but not listed here.

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

18 authors at 3 institutions in 2 countries.

Ana TellecheaBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Ermelindo C LealBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Antonios KafanasBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Michael E AusterBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Sarada KuchibhotlaBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Yana OstrovskyBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Francesco TecilazichBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Dimitrios BaltzisBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Yongjun ZhengBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Eugénia CarvalhoBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Janice M ZabolotnyBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Zuyi WengMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA.
Anastasia PetraMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA.
Arti PatelMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA.
Smaro PanagiotidouMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA.
Leena Pradhan-NabzdykBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Theoharis C TheoharidesMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA.
Aristidis VevesBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA aveves@bidmc.harvard.edu.
Harvard University · USTufts University · USBeth Israel Deaconess Medical Center · US

Funding

Mechanisms of Neuropeptides Action in DiabetesR01DK091949 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI VEVES, ARISTIDIS · 2011 to 2014
$2.6M
Natural History of Peripheral Diabetic NeuropathyR01NS046710 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI VEVES, ARISTIDIS · 2005 to 2009
$1.9M
Role of Neuropeptides in Diabetic Foot ProblemsR01NS066205 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PRADHAN-NABZDYK, LEENA, VEVES, ARISTIDIS · 2010 to 2014
$1.9M
Impaired Wound Healing in Diabetic Foot UlcerationR01DK076937 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI VEVES, ARISTIDIS · 2007 to 2010
$1.4M
NIDDK NIH HHS R01 DK076937NIDDK NIH HHS R01 DK091949NINDS NIH HHS R01 NS046710NINDS NIH HHS R01 NS066205
6 · The paper itself

Abstract

Diabetic foot ulceration is a severe complication of diabetes that lacks effective treatment. Mast cells (MCs) contribute to wound healing, but their role in diabetes skin complications is poorly understood. Here we show that the number of degranulated MCs is increased in unwounded forearm and foot skin of patients with diabetes and in unwounded dorsal skin of diabetic mice (P < 0.05). Conversely, postwounding MC degranulation increases in nondiabetic mice, but not in diabetic mice. Pretreatment with the MC degranulation inhibitor disodium cromoglycate rescues diabetes-associated wound-healing impairment in mice and shifts macrophages to the regenerative M2 phenotype (P < 0.05). Nevertheless, nondiabetic and diabetic mice deficient in MCs have delayed wound healing compared with their wild-type (WT) controls, implying that some MC mediator is needed for proper healing. MCs are a major source of vascular endothelial growth factor (VEGF) in mouse skin, but the level of VEGF is reduced in diabetic mouse skin, and its release from human MCs is reduced in hyperglycemic conditions. Topical treatment with the MC trigger substance P does not affect wound healing in MC-deficient mice, but improves it in WT mice. In conclusion, the presence of nondegranulated MCs in unwounded skin is required for proper wound healing, and therapies inhibiting MC degranulation could improve wound healing in diabetes.

Indexed as

AgedAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NeuropathiesFemaleHumansMaleMast CellsMiceMiddle AgedSkinWound Healing

Identifiers

PMID27207516
PMCPMC4915574
OpenAlexW2320716983

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.