Evidence map›Paper›PMID 33655702›Full record

ArticleJournal of diabetes investigation2021

CIDEC silencing attenuates diabetic nephropathy via inhibiting apoptosis and promoting autophagy.

Gao-Shu Zheng, Yan-Min Tan, Yuan-Yuan Shang, Ya-Peng Liu, Bo-Ang Hu, Di Wang, Lu Han, Zhi-Hao Wang, Wei Zhang, Yun Ti and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  9. Protective Effects ofAntibiotics (Basel, Switzerland) · 2022
    Article
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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

11 authors at 1 institution in 2 countries.

Gao-Shu ZhengThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Yan-Min TanThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Yuan-Yuan ShangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Ya-Peng LiuThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Bo-Ang HuThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Di WangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Lu HanThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Zhi-Hao WangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Wei ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Yun TiThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Ming ZhongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.ORCID https://orcid.org/0000-0002-6229-4943
Shandong University · CN

Funding

National Natural Science Foundation of China 81300168National Natural Science Foundation of China 81900332Natural Science Foundation of Shandong Province ZR2019QH010Science and Technology Planning Project of Wenzhou Science & Technology Bureau of Zhejiang Province of China Y20180128
6 · The paper itself

Abstract

objectiveThe role of cell death-inducing DFF45-like effector C (CIDEC) in insulin resistance has been established, and it is considered to be an important trigger factor for the progression of diabetic nephropathy (DN). We intend to explore whether CIDEC plays an important role in the regulation of DN and its potential mechanism.

methodsHigh-fat diet and low dose streptozotocin were used to establish type 2 diabetic rat model. We investigate the role of CIDEC in the pathogenesis and process of DN through histopathological analysis, western blot and gene silencing. Meanwhile, the effect of CIDEC on renal tubular epithelial cells stimulated by high glucose was also verified.

resultsDM group exhibited glucose and lipid metabolic disturbance, with hypertrophy of kidneys, damaged renal function, increased apoptosis, decreased autophagy, glomerulosclerosis and interstitial fibrosis. CIDEC gene silencing improved metabolic disorder and insulin resistance, alleviated renal hypertrophy and renal function damage, decreased glomerular and tubular apoptosis, increased autophagy and inhibited renal fibrosis. At the cellular level, high glucose stimulation increased CIDEC expression in renal tubular epithelial cells, accompanied by increased apoptosis and decreased autophagy. CIDEC gene silencing can improve autophagy and reduce apoptosis. At the molecular level, CIDEC gene silencing also decreased the expression of early growth response factor (EGR)1 and increased the expression of adipose triglyceride lipase (ATGL).

conclusionCIDEC gene silencing may delay the progression of DN by restoring autophagy activity and inhibiting apoptosis with the participation of EGR1and ATGL.

Indexed as

AcyltransferasesAnimalsApoptosisAutophagyDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic NephropathiesDiet, High-FatEarly Growth Response Protein 1Epithelial CellsGene SilencingKidney TubulesLipaseProteinsRatsRats, Sprague-DawleyAcyltransferasesCidec protein, ratEarly Growth Response Protein 1Egr1 protein, ratLipasePNPLA2 protein, ratProteinsCIDECDiabetic nephropathy

Identifiers

PMID33655702
PMCPMC8354488
OpenAlexW3135760631

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.