Evidence map›Paper›PMID 38288646›Full record

ReviewYonsei medical journal2024

Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.

Se Hee Min, Gil Myoung Kang, Jae Woo Park, Min-Seon Kim

Open access · goldAbstract readReview
In one paragraph

Review in Yonsei medical journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

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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 1 country.

Se Hee MinDivision of Endocrinology and Metabolism, Department of Internal Medicine, Diabetes Center, Asan Medical Center and University of Ulsan College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-9423-3937
Gil Myoung KangAppetite Regulation Laboratory, Asan Institute for Life Science, Seoul, Korea.ORCID https://orcid.org/0000-0002-9398-1893
Jae Woo ParkAppetite Regulation Laboratory, Asan Institute for Life Science, Seoul, Korea.ORCID https://orcid.org/0000-0002-6306-7443
Min-Seon KimDivision of Endocrinology and Metabolism, Department of Internal Medicine, Diabetes Center, Asan Medical Center and University of Ulsan College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-4881-0390
Asan Medical Center · KR

Funding

National Research Foundation of Korea 2020R1A2C3004843National Research Foundation of Korea 2022M3E5E8017213National Research Foundation of Korea 2022R1C1C1012590National Research Foundation of Korea 2022R1C1C2007378
6 · The paper itself

Abstract

Mitochondria function as platforms for bioenergetics, nutrient metabolism, intracellular signaling, innate immunity regulators, and modulators of stem cell activity. Thus, the decline in mitochondrial functions causes or correlates with diabetes mellitus and many aging-related diseases. Upon stress or damage, the mitochondria elicit a series of adaptive responses to overcome stress and restore their structural integrity and functional homeostasis. These adaptive responses to low-level or transient mitochondrial stress promote health and resilience to upcoming stress. Beneficial effects of low-grade mitochondrial stress, termed mitohormesis, have been observed in various organisms, including mammals. Accumulated evidence indicates that treatments boosting mitohormesis have therapeutic potential in various human diseases accompanied by mitochondrial stress. Here, we review multiple cellular signaling pathways and interorgan communication mechanisms through which mitochondrial stress leads to advantageous outcomes. We also discuss the relevance of mitohormesis in obesity, diabetes, metabolic liver disease, aging, and exercise.

Indexed as

Health PromotionMetabolic DiseasesAgingAnimalsExerciseHumansMammalsMitochondriaOxidative StressagingdiabeteshormesisMitochondriaobesitystress

Identifiers

PMID38288646
PMCPMC10827639
OpenAlexW4391112157

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.