↓ Skip to main content

Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway

Overview of attention for article published in Cardiovascular Diabetology, June 2016
Altmetric Badge

About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#32 of 1,000)
  • High Attention Score compared to outputs of the same age (93rd percentile)

Mentioned by

news
3 news outlets
twitter
7 tweeters
facebook
2 Facebook pages

Citations

dimensions_citation
52 Dimensions

Readers on

mendeley
91 Mendeley
citeulike
1 CiteULike
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway
Published in
Cardiovascular Diabetology, June 2016
DOI 10.1186/s12933-016-0397-2
Pubmed ID
Authors

Concepción Peiró, Tania Romacho, Verónica Azcutia, Laura Villalobos, Emilio Fernández, Juan P. Bolaños, Salvador Moncada, Carlos F. Sánchez-Ferrer

Abstract

Hyperglycemia is acknowledged as a pro-inflammatory condition and a major cause of vascular damage. Nevertheless, we have previously described that high glucose only promotes inflammation in human vascular cells previously primed with pro-inflammatory stimuli, such as the cytokine interleukin (IL)1β. Here, we aimed to identify the cellular mechanisms by which high glucose exacerbates the vascular inflammation induced by IL1β. Cultured human aortic smooth muscle cells (HASMC) and isolated rat mesenteric microvessels were treated with IL1β in medium containing 5.5-22 mmol/L glucose. Glucose uptake and consumption, lactate production, GLUT1 levels, NADPH oxidase activity and inflammatory signalling (nuclear factor-κB activation and inducible nitric oxide synthase expression) were measured in HASMC, while endothelium-dependent relaxations to acetylcholine were determined in rat microvessels. Pharmacological inhibition of IL1 receptors, NADPH oxidase and glucose-6-phosphate dehydrogenase (G6PD), as well as silencing of G6PD, were also performed. Moreover, the pentose phosphate pathway (PPP) activity and the levels of reduced glutathione were determined. We found that excess glucose uptake in HASMC cultured in 22 mM glucose only occurred following activation with IL1β. However, the simple entry of glucose was not enough to be deleterious since over-expression of the glucose transporter GLUT1 or increased glucose uptake following inhibition of mitochondrial respiration by sodium azide was not sufficient to trigger inflammatory mechanisms. In fact, besides allowing glucose entry, IL1β activated the PPP, thus permitting some of the excess glucose to be metabolized via this route. This in turn led to an over-activation NADPH oxidase, resulting in increased generation of free radicals and the subsequent downstream pro-inflammatory signalling. Moreover, in rat mesenteric microvessels high glucose incubation enhanced the endothelial dysfunction induced by IL1β by a mechanism which was abrogated by the inhibition of the PPP. A pro-inflammatory stimulus like IL1β transforms excess glucose into a vascular deleterious agent by causing an increase in glucose uptake and its subsequent diversion into the PPP, promoting the pro-oxidant conditions required for the exacerbation of pro-oxidant and pro-inflammatory pathways. We propose that over-activation of the PPP is a crucial mechanism for the vascular damage associated to hyperglycemia.

Twitter Demographics

The data shown below were collected from the profiles of 7 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 91 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 91 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 16 18%
Student > Master 13 14%
Student > Bachelor 10 11%
Researcher 7 8%
Student > Doctoral Student 7 8%
Other 19 21%
Unknown 19 21%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 20 22%
Agricultural and Biological Sciences 16 18%
Medicine and Dentistry 16 18%
Immunology and Microbiology 5 5%
Nursing and Health Professions 3 3%
Other 9 10%
Unknown 22 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 29. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 November 2019.
All research outputs
#841,052
of 17,429,432 outputs
Outputs from Cardiovascular Diabetology
#32
of 1,000 outputs
Outputs of similar age
#18,841
of 273,276 outputs
Outputs of similar age from Cardiovascular Diabetology
#1
of 1 outputs
Altmetric has tracked 17,429,432 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 95th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,000 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.6. This one has done particularly well, scoring higher than 97% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 273,276 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 93% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them