Evidence map›Paper›PMID 29574544›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2018

Preservation of renal function in chronic diabetes by enhancing glomerular glucose metabolism.

Weier Qi, Qian Li, Daniel Gordin, George L King

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. The Role of PKM2 in Diabetic Microangiopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Differences in Serum Amino Acid Phenotypes Among Patients with Diabetic Nephropathy, Hypertensive Nephropathy, and Chronic Nephritis.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
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

4 authors at 1 institution in 2 countries.

Weier QiResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Qian LiResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Daniel GordinResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
George L KingResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. George.King@Joslin.harvard.edu.
Joslin Diabetes Center · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Pyruvate kinase M2 levels and activation as protective factors for diabetic nephropathyDP3DK112192 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 2016 to 2016
$2.3M
Juvenile Diabetes Research Foundation 17-2011-47Juvenile Diabetes Research Foundation 18-2008-363Juvenile Diabetes Research Foundation 8-2005-358NIDDK NIH HHS DP3 DK112192NIDDK NIH HHS P30 DK036836NIH HHS 1DP3DK112192-01NIH HHS P30DK036836
6 · The paper itself

Abstract

Diabetic nephropathy (DN) affects approximately 30-40% of patients with type 1 (T1DM) and type 2 diabetes (T2DM). It is a major cause of end-stage renal disease (ESRD) for the developed world. Hyperglycemia and genetics are major causal factors for the initiation and progression of DN. Multiple abnormalities in glucose and mitochondrial metabolism induced by diabetes likely contribute to the severity of DN. Recent clinical studies in people with extreme duration of T1DM (> 50 years, Joslin Medalist Study) have supported the importance of endogenous protective factors to neutralize the toxic effects of hyperglycemia on renal and other vascular tissues. Using renal glomeruli from these patients (namely Medalists) with and without DN, we have shown the importance of increased glycolytic flux in decreasing the accumulation of glucose toxic metabolites, improving mitochondrial function, survival of glomerular podocytes, and reducing glomerular pathology. Activation of a key glycolytic enzyme, pyruvate kinase M2 (PKM2), resulted in the normalization of renal hemodynamics and mitochondrial and glomerular dysfunction, leading to the mitigation of glomerular pathologies in several mouse models of DN.

Indexed as

AnimalsChronic DiseaseDiabetic NephropathiesGlucoseHumansKidneyGlucoseDiabetic nephropathyGlucose metabolismGlycolysisMetabolitesPKM2

Identifiers

PMID29574544
PMCPMC7132623
OpenAlexW2794386140

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.