Evidence map›Paper›PMID 31391172›Full record

ArticleDiabetes2019

Elevated Thrombospondin 2 Contributes to Delayed Wound Healing in Diabetes.

Britta Kunkemoeller, Tara Bancroft, Hao Xing, Aaron H Morris, Amelia K Luciano, Jason Wu, Carlos Fernandez-Hernando, Themis R Kyriakides

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  10. Targeting hypoxia and thrombospondin-2 in diabetic wound healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  11. Review
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  13. Circulating thrombospondin-2 level for identifying individuals with rapidly declining kidney function trajectory in type 2 diabetes: a prospective study of the Hong Kong West Diabetes Registry.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
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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

8 authors at 1 institution in 1 country.

Britta KunkemoellerDepartment of Pathology, Yale University School of Medicine, New Haven, CT.
Tara BancroftDepartment of Pathology, Yale University School of Medicine, New Haven, CT.
Hao XingInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT.
Aaron H MorrisInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT.
Amelia K LucianoInterdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT.
Jason WuDepartment of Pathology, Yale University School of Medicine, New Haven, CT.
Carlos Fernandez-HernandoDepartment of Pathology, Yale University School of Medicine, New Haven, CT.
Themis R KyriakidesDepartment of Pathology, Yale University School of Medicine, New Haven, CT themis.kyriakides@yale.edu.ORCID 0000-0002-1937-5764
Yale University · US

Funding

Surgery / Physiology CoreP01HL107205 · NHLBI · YALE UNIVERSITY · PI SCHWARTZ, MARTIN A · 2012 to 2022
$18.8M
MCP-1 and attenuation of the foreign body responseR01GM072194 · NIGMS · YALE UNIVERSITY · PI KYRIAKIDES, THEMIS R · 2005 to 2018
$4.7M
NHLBI NIH HHS P01 HL107205NIGMS NIH HHS R01 GM072194
6 · The paper itself

Abstract

Impaired wound healing is a major complication of diabetes, and despite the associated risks, treatment strategies for diabetic wounds remain limited. This is due, in part, to an incomplete understanding of the underlying pathological mechanisms, including the effects of hyperglycemia on components of the extracellular matrix (ECM). In the current study, we explored whether the expression of thrombospondin 2 (TSP2), a matricellular protein with a demonstrated role in response to injury, was associated with delayed healing in diabetes. First, we found that TSP2 expression was elevated in diabetic mice and skin from patients with diabetes. Then, to determine the contribution of TSP2 to impaired healing in diabetes, we developed a novel diabetic TSP2-deficient model. Though the TSP2-deficient mice developed obesity and hyperglycemia comparable with diabetic control mice, they exhibited significantly improved healing, characterized by accelerated reepithelialization and increased granulation tissue formation, fibroblast migration, and blood vessel maturation. We further found that hyperglycemia increased TSP2 expression in fibroblasts, the major cellular source of TSP2 in wounds. Mechanistically, high glucose increased activation of the hexosamine pathway and nuclear factor-κB signaling to elevate TSP2 expression. Our studies demonstrate that hyperglycemia-induced TSP2 expression contributes to impaired healing in diabetes.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FibroblastsHumansMiceMice, KnockoutNF-kappa BSignal TransductionSkinThrombospondin 2ThrombospondinsWound HealingBlood GlucoseNF-kappa BThrombospondin 2Thrombospondins

Identifiers

PMID31391172
PMCPMC6754242
OpenAlexW2965527677

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.