Evidence map›Paper›PMID 33041516›Full record

ArticleJournal of clinical biochemistry and nutrition2020

Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease.

Yuki Niida, Masashi Masuda, Yuichiro Adachi, Aika Yoshizawa, Hirokazu Ohminami, Yuki Mori, Kohta Ohnishi, Hisami Yamanaka-Okumura, Takayuki Uchida, Takeshi Nikawa and 3 more

Abstract read
In one paragraph

Article in Journal of clinical biochemistry and nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. 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

13 authors.

Yuki NiidaDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Masashi MasudaDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Yuichiro AdachiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Aika YoshizawaDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Hirokazu OhminamiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Yuki MoriDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Kohta OhnishiDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Hisami Yamanaka-OkumuraDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Takayuki UchidaDepartment of Nutritional Physiology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Takeshi NikawaDepartment of Nutritional Physiology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Hironori YamamotoDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Makoto MiyazakiDivision of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, Aurora, Colorado 80045, USA.
Yutaka TaketaniDepartment of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.

Funding

The role of MLKL in the regulation of vascular calcification in CKDR01HL132318 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2016 to 2025
$3.8M
The contributory role of microbial metabolite in the pathogenesis of CKD-dependent vascular calcificationR01HL133545 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2018 to 2021
$1.9M
The Role of Stearate in The Regulation of Vascular Calcification in Chronic Kidney DiseaseR01HL117062 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL117062NHLBI NIH HHS R01 HL132318NHLBI NIH HHS R01 HL133545
6 · The paper itself

Abstract

Skeletal muscle atrophy is associated with mortality and poor prognosis in patients with chronic kidney disease (CKD). However, underlying mechanism by which CKD causes muscle atrophy has not been completely understood. The quality of lipids (lipoquality), which is defined as the functional features of diverse lipid species, has recently been recognized as the pathology of various diseases. In this study, we investigated the roles of the stearoyl-CoA desaturase (SCD), which catalyzes the conversion of saturated fatty acids into monounsaturated fatty acids, in skeletal muscle on muscle atrophy in CKD model animals. In comparison to control rats, CKD rats decreased the SCD activity and its gene expression in atrophic gastrocnemius muscle. Next, oleic acid blocked the reduction of the thickness of C2C12 myotubes and the increase of the endoplasmic reticulum stress induced by SCD inhibitor. Furthermore, endoplasmic reticulum stress inhibitor ameliorated CKD-induced muscle atrophy (the weakness of grip strength and the decrease of muscle fiber size of gastrocnemius muscle) in mice and the reduction of the thickness of C2C12 myotubes by SCD inhibitor. These results suggest that the repression of SCD activity causes muscle atrophy through excessive endoplasmic reticulum stress in CKD.

Indexed as

chronic kidney diseaseendoplasmic reticulum stresssaturated fatty acidskeletal muscle atrophystearoyl-CoA desaturase

Identifiers

PMID33041516
PMCPMC7533850

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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.