Evidence map›Paper›PMID 24507996›Full record

ReviewTrends in endocrinology and metabolism: TEM2014

Emerging roles of hematopoietic cells in the pathobiology of diabetic complications.

Hideto Kojima, Jongoh Kim, Lawrence Chan

Abstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Diabetes Induces a Transcriptional Signature in Bone Marrow-Derived CD34International journal of molecular sciences · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Diabetic corneal neuropathy: clinical perspectives.Clinical ophthalmology (Auckland, N.Z.) · 2018
    Review
  20. Diabetes-mediated myelopoiesis and the relationship to cardiovascular risk.Annals of the New York Academy of Sciences · 2017
    Review
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

3 authors at 1 institution in 2 countries.

Hideto KojimaDepartments of Medicine and Molecular and Cellular Biology, and the Diabetes and Endocrinology Research Center, Baylor College of Medicine, Houston, Texas 77030, USA; Department of Stem Cell Biology and Regenerative Medicine, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Jongoh KimDepartments of Medicine and Molecular and Cellular Biology, and the Diabetes and Endocrinology Research Center, Baylor College of Medicine, Houston, Texas 77030, USA.
Lawrence ChanDepartments of Medicine and Molecular and Cellular Biology, and the Diabetes and Endocrinology Research Center, Baylor College of Medicine, Houston, Texas 77030, USA. Electronic address: lchan@bcm.edu.
Baylor College of Medicine · US

Funding

Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
MODELS FOR ATHEROSCLEROSIS RESEARCHR01HL051586 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 1994 to 2014
$5.5M
Molecular Medicine Scholars Training GrantT32HL066991 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2002 to 2012
$2.1M
NHLBI NIH HHS R01 HL051586NHLBI NIH HHS R01-HL051586NHLBI NIH HHS T32 HL066991NHLBI NIH HHS T32-HL066991NIDDK NIH HHS P30 DK079638NIDDK NIH HHS P30-DK079638
6 · The paper itself

Abstract

Diabetic complications encompass macrovascular events, mainly the result of accelerated atherosclerosis, and microvascular events that strike the eye (retinopathy), kidney (nephropathy), and nervous system (neuropathy). The traditional view is that hyperglycemia-induced dysregulated biochemical pathways cause injury and death of cells intrinsic to the organs affected. There is emerging evidence that diabetes compromises the function of the bone marrow (BM), producing a stem cell niche-dependent defect in hematopoietic stem cell mobilization. Furthermore, dysfunctional BM-derived hematopoietic cells contribute to diabetic complications. Thus, BM cells are not only a victim but also an accomplice in diabetes and diabetic complications. Understanding the underlying molecular mechanisms may lead to the development of new therapies to prevent and/or treat diabetic complications by specifically targeting these perpetrators.

Indexed as

AnimalsBone MarrowDiabetes ComplicationsHematopoietic Stem Cell MobilizationHumansHyperglycemiabone marrowcomplicationsdiabetes mellitusdiabetic nephropathydiabetic neuropathydiabetic retinopathyhematopoietic cells

Identifiers

PMID24507996
PMCPMC3975817
OpenAlexW1969281194

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.