Evidence mapPaperPMID 35601149Full record

ArticleBioMed research international2022

Artemether Alleviates Diabetic Kidney Disease by Modulating Amino Acid Metabolism.

Guangli Rong, Wenci Weng, Jingting Huang, Yijun Chen, Xuewen Yu, Rui Yuan, Xiufen Gu, Xia Wu, Yuchun Cai, Pengxun Han and 3 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. World journal of diabetes · 2023
    Article
  8. Article
  9. Review
  10. SUPPRESION OF MITOCHONDRIAL RESPIRATION IS A FEATURE OF CELLULAR GLUCOSE TOXICITY.Transactions of the American Clinical and Climatological Association · 2023
    Article
  11. 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 at 1 institution in 1 country.

Guangli RongDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.ORCID https://orcid.org/0000-0001-5054-2383
Wenci WengDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Jingting HuangDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Yijun ChenDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Xuewen YuDepartment of Pathology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Rui YuanDepartment of Clinical Laboratory, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Xiufen GuDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Xia WuDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Yuchun CaiDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Pengxun HanDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Mumin ShaoDepartment of Pathology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.
Huili SunDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.ORCID https://orcid.org/0000-0002-7101-1087
Na GeDepartment of Nephrology, The Fourth Clinical Medical School of Guangzhou University of Chinese Medicine, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033 Guangdong, China.ORCID https://orcid.org/0000-0003-3535-1874
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is a worldwide metabolic disease with rapid growing incidence, characterized by hyperglycemia. Diabetic kidney disease (DKD), the leading cause of chronic kidney disease (CKD), has a high morbidity according to the constantly increasing diabetic patients and always develops irreversible deterioration of renal function. Though different in pathogenesis, clinical manifestations, and therapies, both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) can evolve into DKD. Since amino acids are both biomarkers and causal agents, rarely report has been made about its metabolism which lies in T1DM- and T2DM-related kidney disease. This study was designed to investigate artemether in adjusting renal amino acid metabolism in T1DM and T2DM mice. Artemether was applied as treatment in streptozotocin (STZ) induced T1DM mice and db/db T2DM mice, respectively. Artemether-treated mice showed lower FBG and HbA1c and reduced urinary albumin excretion, as well as urinary NAG. Both types of diabetic mice showed enlarged kidneys, as confirmed by increased kidney weight and the ratio of kidney weight to body weight. Artemether normalized kidney size and thus attenuated renal hypertrophy. Kidney tissue UPLC-MS analysis showed that branched-chain amino acids (BCAAs) and citrulline were upregulated in diabetic mice without treatment and downregulated after being treated with artemether. Expressions of glutamine, glutamic acid, aspartic acid, ornithine, glycine, histidine, phenylalanine and threonine were decreased in both types of diabetic mice whereas they increased after artemether treatment. The study demonstrates the initial evidence that artemether exerted renal protection in DKD by modulating amino acid metabolism.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic NephropathiesAmino AcidsAnimalsArtemetherChromatography, LiquidHumansKidneyMiceTandem Mass SpectrometryAmino AcidsArtemether

Identifiers

PMID35601149
PMCPMC9117059
OpenAlexW4280643568

What Socratic 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 Socratic graph.