Evidence map›Paper›PMID 35468098›Full record

ArticleAging2022

Endothelin-1-mediated miR-let-7g-5p triggers interlukin-6 and TNF-α to cause myopathy and chronic adipose inflammation in elderly patients with diabetes mellitus.

Chung-Huang Tsai, Pei-Ju Huang, I T Lee, Chien-Min Chen, Min Huan Wu

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
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  5. Review
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  9. The Association Between Sarcopenia and Diabetes: From Pathophysiology Mechanism to Therapeutic Strategy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Chung-Huang TsaiDepartment of Family Medicine, Chung-Kang Branch, Cheng Ching Hospital, Taichung, Taiwan.
Pei-Ju HuangDepartment of Family Medicine, Changhua Christian Hospital, Changhua, Taiwan.
I T LeeDivision of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Chien-Min ChenDivision of Traditional Chinese Medical, Sinying Hospital, Tainan, Taiwan.
Min Huan WuBachelor of Science in Senior Wellness and Sport Science, Tunghai University, Taiwan.
Tunghai University · TWChanghua Christian Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes and sarcopenia are verified as mutual relationships, which seriously affect the quality of life of the elderly. Endothelin-1 is well investigated, is elevated in patients with diabetes, and is related to muscle cellular senescence and fibrosis. However, the mechanism of ET-1 between diabetes and myopathy is still unclear. The aim of this study was to evaluate the prevalence of sarcopenia in the elderly with diabetes and to clarify its relationship with ET-1 molecular biological mechanism, progress as well as changes in muscle and fat.

methodsWe recruited 157 type 2 diabetes patients over 55 years old and investigated the prevalence of sarcopenia in diabetes patients and examined the association of ET-1 alterations with HbA1c, creatinine, or AMS/ht2. Next, sought to determine how ET-1 regulates inflammation in muscle cells by western blot and qPCR assay. Using XF Seahorse Technology, we directly quantified mitochondrial bioenergetics in 3T3-L1 cells.

resultsET-1 was positively correlated with HbA1c, creatinine levels, and duration of disease, and negatively correlated with AMS/ht2. We found that ET-1 dose-dependently induces tumor necrosis factor-α (TNF-α) and interleukin (IL)-6β expression through the PI3K/AKT, and NF-κB signaling pathways in C2C12 cells. Also identified that TNF-α, IL-6β, and visfatin releases were found in co-cultured with conditioned medium of ET-1/C2C12 in 3T3-L1 cells. ET-1 also reduces the energy metabolism of fat and induces micro-environment inflammation which causes myopathy. ET-1 also suppresses miR-let-7g-5p expression in myocytes and adipocytes.

conclusionWe describe a new mechanism of ET-1 triggering chronic inflammation in patients with hyperglycemia.

Indexed as

Diabetes Mellitus, Type 2MicroRNAsMuscular DiseasesSarcopeniaAgedCreatinineEndothelin-1Glycated HemoglobinHumansInflammationPhosphatidylinositol 3-KinasesQuality of LifeTumor Necrosis Factor-alphaCreatinineEndothelin-1Glycated HemoglobinMicroRNAsPhosphatidylinositol 3-KinasesTumor Necrosis Factor-alphadiabetesendothelin-1 (ET-1)hyperglycemiainterleukin-6miRNAsarcopeniaTNF-α

Identifiers

PMID35468098
PMCPMC9085227
OpenAlexW4224587826

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.