Evidence map›Paper›PMID 23637966›Full record

ArticlePloS one2013

Celastrol, an NF-κB inhibitor, improves insulin resistance and attenuates renal injury in db/db mice.

Jung Eun Kim, Mi Hwa Lee, Deok Hwa Nam, Hye Kyoung Song, Young Sun Kang, Ji Eun Lee, Hyun Wook Kim, Jin Joo Cha, Young Youl Hyun, Sang Youb Han and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
33.4field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Molecular Therapeutics for Diabetic Kidney Disease: An Update.International journal of molecular sciences · 2024
    Review
  14. Lipids: A Major Culprit in Diabetic Nephropathy.Current diabetes reviews · 2024
    Review
  15. Review
  16. Frontiers in pharmacology · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Review

20 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

13 authors at 5 institutions in 1 country.

Jung Eun KimDepartment of Internal Medicine, Division of Nephrology, Korea University, Ansan City, Kyungki-Do, Korea.
Mi Hwa Lee
Deok Hwa Nam
Hye Kyoung Song
Young Sun Kang
Ji Eun Lee
Hyun Wook Kim
Jin Joo Cha
Young Youl Hyun
Sang Youb Han
Kum Hyun Han
Jee Young Han
Dae Ryong Cha
Korea University · KRInje University · KRWonkwang University · KRInha University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-κB pathway plays an important role in chronic inflammatory and autoimmune diseases. Recently, NF-κB has also been suggested as an important mechanism linking obesity, inflammation, and metabolic disorders. However, there is no current evidence regarding the mechanism of action of NF-κB inhibition in insulin resistance and diabetic nephropathy in type 2 diabetic animal models. We investigated the effects of the NF-κB inhibitor celastrol in db/db mice. The treatment with celastrol for 2 months significantly lowered fasting plasma glucose (FPG), HbA1C and homeostasis model assessment index (HOMA-IR) levels. Celastrol also exhibited significant decreases in body weight, kidney/body weight and adiposity. Celastrol reduced insulin resistance and lipid abnormalities and led to higher plasma adiponectin levels. Celastrol treatment also significantly mitigated lipid accumulation and oxidative stress in organs including the kidney, liver and adipose tissue. The treated group also exhibited significantly lower creatinine levels and urinary albumin excretion was markedly reduced. Celastrol treatment significantly lowered mesangial expansion and suppressed type IV collagen, PAI-1 and TGFβ1 expressions in renal tissues. Celastrol also improved abnormal lipid metabolism, oxidative stress and proinflammatory cytokine activity in the kidney. In cultured podocytes, celastrol treatment abolished saturated fatty acid-induced proinflammatory cytokine synthesis. Taken together, celastrol treatment not only improved insulin resistance, glycemic control and oxidative stress, but also improved renal functional and structural changes through both metabolic and anti-inflammatory effects in the kidney. These results suggest that targeted therapy for NF-κB may be a useful new therapeutic approach for the management of type II diabetes and diabetic nephropathy.

Indexed as

Insulin ResistanceAdipose TissueAlbuminuriaAnimalsCells, CulturedCytokinesDiabetes Mellitus, ExperimentalFatty AcidsGlycated HemoglobinInflammation MediatorsKidneyKidney Function TestsKidney GlomerulusLipid PeroxidationLipidsLivercelastrolCytokinesFatty AcidsGlycated HemoglobinInflammation MediatorsLipidsNF-kappa BPentacyclic TriterpenesTriterpenes

Identifiers

PMID23637966
PMCPMC3637455
OpenAlexW2019024943

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.