Evidence map›Paper›PMID 30307158›Full record

ReviewJournal of molecular endocrinology2018

The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseases

Hyon-Seung Yi, Joon Young Chang, Minho Shong

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Exercise elicits mitonuclear protein imbalance and UPRJournal of physiology and biochemistry · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Coenzyme Q10 and Obesity: An Overview.Antioxidants (Basel, Switzerland) · 2025
    Review
  9. Advances in Management of Mitochondrial Myopathies.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. UNC-49 is a redox-sensitive GABAScience advances · 2023
    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

3 authors at 1 institution in 1 country.

Hyon-Seung YiResearch Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Korea
Joon Young ChangResearch Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Korea
Minho ShongResearch Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Korea
Chungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria perform essential roles as crucial organelles for cellular and systemic energy homeostasis, and as signaling hubs, which coordinate nuclear transcriptional responses to the intra- and extra-cellular environment. Complex human diseases, including diabetes, obesity, fatty liver disease and aging-related degenerative diseases are associated with alterations in mitochondrial oxidative phosphorylation (OxPhos) function. However, a recent series of studies in animal models have revealed that an integrated response to tolerable mitochondrial stress appears to render cells less susceptible to subsequent aging processes and metabolic stresses, which is a key feature of mitohormesis. The mitochondrial unfolded protein response (UPRmt) is a central part of the mitohormetic response and is a retrograde signaling pathway, which utilizes the mitochondria-to-nucleus communication network. Our understanding of the UPRmt has contributed to elucidating the role of mitochondria in metabolic adaptation and lifespan regulation. In this review, we discuss and integrate recent data from the literature on the present status of mitochondrial OxPhos function in the development of metabolic diseases, relying on evidence from human and other animal studies, which points to alterations in mitochondrial function as a key factor in the regulation of metabolic diseases and conclude with a discussion on the specific roles of UPRmt and mitohormesis as a novel therapeutic strategy for the treatment of obesity and insulin resistance.

Indexed as

AnimalsHumansInsulin ResistanceMetabolic DiseasesMitochondriaOxidative PhosphorylationSignal TransductionUnfolded Protein Responsediabetesinsulin resistancemitochondriamitochondrial unfolded protein responseoxidative phosphorylation

Identifiers

PMID30307158
PMCPMC6145237
OpenAlexW2805958828

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.