Evidence map›Paper›PMID 23847051›Full record

ArticleHuman molecular genetics2013

Curcumin facilitates a transitory cellular stress response in Trembler-J mice.

Yuji Okamoto, Davut Pehlivan, Wojciech Wiszniewski, Christine R Beck, G Jackson Snipes, James R Lupski, Mehrdad Khajavi

Open access · greenAbstract read
In one paragraph

Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Charcot-Marie-Tooth disease type 1E: Clinical Natural History and Molecular Impact ofmedRxiv : the preprint server for health sciences · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Mechanisms and Treatments in Demyelinating CMT.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

7 authors at 1 institution in 1 country.

Yuji OkamotoDepartment of Molecular and Human Genetics.
Davut Pehlivan
Wojciech Wiszniewski
Christine R Beck
G Jackson Snipes
James R Lupski
Mehrdad Khajavi
Boston Children's Hospital · US

Funding

Nonrecurrent rearrangements, genome architecture and neurodegenerative disease.R01NS058529 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI LUPSKI, JAMES R. · 2009 to 2017
$5.0M
Mutidisciplinary Training;Brain Disorders &DevelopmentT32NS043124 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SWANN, JOHN WILLIAM · 2002 to 2021
$4.6M
Genome analysis to elucidate molecular mechanisms for peripheral neuropathiesK23NS078056 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI WISZNIEWSKI, WOJCIECH KRZYSZTOF · 2012 to 2016
$783k
NINDS NIH HHS K23 NS078056NINDS NIH HHS K23NS078056NINDS NIH HHS R01 NS058529NINDS NIH HHS R01NS058529NINDS NIH HHS T32 NS043124
6 · The paper itself

Abstract

We have previously shown that oral administration of curcumin significantly decreases the percentage of apoptotic Schwann cells and partially mitigates the severe neuropathy phenotype of the Trembler-J (Tr-J) mouse model in a dose-dependent manner. Here we compared the gene expression in sciatic nerves of 2-week-old pups and adult Tr-J with the same age groups of wild-type mice and found a significant increase in gene expression for hypoxia, inflammatory response and heat-shock proteins, the latter specifically the Hsp70 family, in Tr-J mice. We also detected an activation of different branches of unfolded protein responses (UPRs) in Tr-J mice. Administering curcumin results in lower expression of UPR markers suggesting it relieves endoplasmic reticulum (ER) cell stress sensors in sciatic nerves of Tr-J mice while the level of heat-shock proteins stays comparable to untreated Tr-J mice. We further tested if Hsp70 levels could influence the severity of the Tr-J neuropathy. Notably, reduced dosage of the Hsp70 strongly potentiates the severity of the Tr-J neuropathy, though the absence of Hsp70 had little effect in wild-type mice. In aggregate, these data provide further insights into the pathological disease mechanisms caused by myelin gene mutations and further support the exploration of curcumin as a therapeutic approach for selected forms of inherited neuropathy and potentially for other genetic diseases due to ER-retained mutants.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCurcuminDisease Models, AnimalEndoplasmic Reticulum StressFemaleGene Expression Regulation, DevelopmentalHSP70 Heat-Shock ProteinsMaleMiceMice, Inbred C57BLMice, Mutant StrainsMutationMyelin ProteinsPeripheral Nervous System DiseasesSciatic NerveAnti-Inflammatory Agents, Non-SteroidalCurcuminHSP70 Heat-Shock ProteinsMyelin ProteinsPmp22 protein, mouse

Identifiers

PMID23847051
PMCPMC3820132
OpenAlexW2114834554

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.