Evidence map›Paper›PMID 34103347›Full record

ArticleDiabetes2021

The Attenuation of Diabetic Nephropathy by Annexin A1 via Regulation of Lipid Metabolism Through the AMPK/PPARα/CPT1b Pathway.

Liang Wu, Changjie Liu, Dong-Yuan Chang, Rui Zhan, Mingming Zhao, Sin Man Lam, Guanghou Shui, Ming-Hui Zhao, Lemin Zheng, Min Chen

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 113 citations in OpenAlex.

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  6. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  7. Exploration (Beijing, China) · 2026
    Article
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12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Liang WuRenal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China.ORCID 0000-0001-6904-259X
Changjie LiuInstitute of Cardiovascular Sciences, Institute of Systems Biomedicine, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University Health Science Center, Beijing, China.
Dong-Yuan ChangRenal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China.
Rui ZhanInstitute of Cardiovascular Sciences, Institute of Systems Biomedicine, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University Health Science Center, Beijing, China.
Mingming ZhaoInstitute of Cardiovascular Sciences, Institute of Systems Biomedicine, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University Health Science Center, Beijing, China.
Sin Man LamState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Guanghou ShuiState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.ORCID 0000-0002-1621-9643
Ming-Hui ZhaoRenal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China.
Lemin ZhengInstitute of Cardiovascular Sciences, Institute of Systems Biomedicine, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University Health Science Center, Beijing, China chenmin74@sina.com zhengl@bjmu.edu.cn.ORCID 0000-0003-4473-6936
Min ChenRenal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China chenmin74@sina.com zhengl@bjmu.edu.cn.ORCID 0000-0002-6413-6973
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNPeking University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and abnormal metabolism play important roles in the pathogenesis of diabetic nephropathy (DN). Annexin A1 (ANXA1) contributes to inflammation resolution and improves metabolism. In this study, we assess the effects of ANXA1 in diabetic mice and proximal tubular epithelial cells (PTECs) treated with high glucose plus palmitate acid (HGPA) and explore the association of ANXA1 with lipid accumulation in patients with DN. It is found that ANXA1 deletion aggravates renal injuries, including albuminuria, mesangial matrix expansion, and tubulointerstitial lesions in high-fat diet/streptozotocin-induced diabetic mice. ANXA1 deficiency promotes intrarenal lipid accumulation and drives mitochondrial alterations in kidneys. In addition, Ac2-26, an ANXA1 mimetic peptide, has a therapeutic effect against lipid toxicity in diabetic mice. In HGPA-treated human PTECs, ANXA1 silencing causes FPR2/ALX-driven deleterious effects, which suppress phosphorylated Thr

Indexed as

AMP-Activated Protein KinasesAnimalsAnnexin A1Carnitine O-PalmitoyltransferaseCase-Control StudiesCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesHumansLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutPPAR alphaSignal TransductionAMP-Activated Protein KinasesAnnexin A1Carnitine O-PalmitoyltransferaseCPT1B protein, humanCPT1B protein, mousePPAR alphaStreptozocin

Identifiers

PMID34103347
OpenAlexW3171466189

What OpenQuestion holds

Textmetadata
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.