Evidence map›Paper›PMID 41275961›Full record

ArticleJournal of advanced research2026

ANXA1 improves mitochondrial homeostasis through uncoupling protein 1 in diabetic nephropathy.

Zi-Han Li, Lu Fang, Liang Wu, Dong-Yuan Chang, Manyuan Dong, Liang Ji, Qi Zhang, Ming-Hui Zhao, Sydney C W Tang, Lemin Zheng and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Zi-Han LiRenal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Department of Nephrology, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China; Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China.
Lu FangThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Liang WuRenal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Department of Nephrology, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China; Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China.
Dong-Yuan ChangRenal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Department of Nephrology, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China; Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China.
Manyuan DongThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Liang JiThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Qi ZhangThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Ming-Hui ZhaoRenal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Department of Nephrology, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China; Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Peking-Tsinghua Center for Life Sciences, Beijing 100034, China.
Sydney C W TangDivision of Nephrology, Department of Medicine, School of Clinical Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
Lemin ZhengThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China; Beijing Tiantan Hospital, China National Clinical Research Center for Neurological Diseases, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Tiantan Xili, Chongwen District, Beijing 100050, China. Electronic address: zhengl@bjmu.edu.cn.
Min ChenRenal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China; Department of Nephrology, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China; Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, China. Electronic address: chenmin74@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDiabetic nephropathy (DN) is a major public health concern. Our previous study found that annexin A1 (ANXA1) alleviated DN by improving mitochondrial homeostasis. However, the underlying mechanism is not fully clear yet.

objectivesThis study aimed to explore mechanisms by which ANXA1 improves mitochondrial homeostasis and identify novel therapeutic targets for DN.

methodsDiabetic Anxa1

resultsTranscriptomics revealed that Ucp1 was the most significantly downregulated mitochondria-associated gene in kidneys of diabetic Anxa1-KO mice. Functional validation demonstrated that local overexpression of Ucp1 in kidneys alleviated urine albumin-to-creatine ratio (uACR), kidney injuries in histopathology and mitochondrial fission in Anxa1-KO diabetic mice. In vitro, UCP1 silencing abolished the improvements of human recombinant ANXA1 on high glucose (HG)-induced inflammation, fibrosis and mitochondrial dysfunction in PTECs. Silencing/overexpression of ANXA1 reduced/increased the stability of transcription factor GATA binding protein 3 (GATA3) in HK-2 cells under HG conditions, respectively. GATA3 could bind to the proximal promoter region of UCP1, thereby enhancing its transcriptional activity. UCP1 was significantly upregulated in kidneys of DN patients and mice. UCP1 deficiency reduced renal cardiolipin and exacerbated diabetes-induced kidney injury, including aggravated uACR, interstitial inflammation and fibrosis, and enhanced mitochondrial fission. Mechanistically, UCP1 upregulated CRLS1 by modulating aristaless-related homeobox (ARX), thereby promoting cardiolipin biosynthesis and reducing mitochondrial fission. Therapeutically, pharmacological upregulation of UCP1 by CL316243 attenuated established DN in db/db mice.

conclusionANXA1 stabilized GATA3 to upregulate UCP1, which promoted cardiolipin biosynthesis through the ARX/CRLS1 axis, inhibited mitochondrial fission, thereby alleviated DN. This study highlighted the therapeutic potential of targeting UCP1 in DN.

Indexed as

Annexin A1Diabetic NephropathiesMitochondriaUncoupling Protein 1AnimalsDiabetes Mellitus, ExperimentalHomeostasisHumansKidneyMaleMiceMice, Inbred C57BLMice, KnockoutAnnexin A1annexin A1, mouseUcp1 protein, mouseUncoupling Protein 1Annexin A1Cardiolipin synthase 1Diabetic nephropathyGATA binding protein 3Mitochondrial dynamicsUncoupling protein 1

Identifiers

PMID41275961
PMCPMC13453871

What OpenQuestion 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 OpenQuestion graph.