Evidence map›Paper›PMID 31402399›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2019

Progranulin alleviates podocyte injury via regulating CAMKK/AMPK-mediated autophagy under diabetic conditions.

Di Zhou, Meng Zhou, Ziying Wang, Yi Fu, Meng Jia, Xiaojie Wang, Min Liu, Yan Zhang, Yu Sun, Yabin Zhou and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  16. Article
  17. Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Article
  20. Antioxidants (Basel, Switzerland) · 2021
    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

13 authors at 1 institution in 1 country.

Di ZhouDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Meng ZhouDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Ziying WangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Yi FuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Meng JiaDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Xiaojie WangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Min LiuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Yan ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Yu SunDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Yabin ZhouDepartment of Pathogenic Biology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Yi LuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, 250012, People's Republic of China.
Wei TangDepartment of Pathogenic Biology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China. weitang@sdu.edu.cn.
Fan YiDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China. fanyi@sdu.edu.cn.ORCID 0000-0001-8634-9788
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Podocyte injury is considered a major contributor to the development of diabetic nephropathy (DN). Therefore, identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Recent studies have indicated that autophagy is a key homeostatic mechanism to maintaining podocyte integrity and function. This study was to elucidate the role of progranulin (PGRN), a secreted glycoprotein, in the modulation of podocyte autophagic process and podocyte injury under a diabetic condition. PGRN was downregulated in the kidney from diabetic mice and podocytes under a high-glucose (HG) condition. PGRN deficiency exacerbated the renal dysfunction and glomerular structural alterations. In vitro, treatment with recombinant human PGRN (rPGRN) attenuated HG-induced podocyte injury accompanied by enhanced autophagy. Inhibition of autophagy disturbed the protective effects of PGRN in HG-induced podocytotoxicity. Furthermore, PGRN induced autophagy via the PGRN-CAMKK-AMPK pathway. Collectively, our data identified the protective role of PGRN in podocyte injury via restoring autophagy and activating the CAMKK-AMPK pathway, which may pave the road to new therapeutic modalities for the treatment of diabetic nephropathy. KEY MESSAGES: • PGRN level is reduced in kidney of diabetic mice and high-glucose-treated podocytes. • PGRN deficiency exacerbates renal injury in diabetic mice. • PGRN protects against high-glucose-induced podocyte injury. • PGRN restores high-glucose-inhibited autophagy in podocytes. • CAMKK-AMPK pathway is required for the protective role of PGRN in podocyte injury.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisCalcium-Calmodulin-Dependent Protein Kinase KinaseCells, CulturedDiabetes Mellitus, ExperimentalFlow CytometryFluorescent Antibody TechniqueHumansKidney GlomerulusMiceMice, Inbred C57BLMicroscopy, ConfocalMicroscopy, Electron, TransmissionPodocytesProgranulinsAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseProgranulinsAutophagyCAMKK-AMPK pathwayDiabetic nephropathyPGRNPodocyte

Identifiers

PMID31402399
OpenAlexW2976391238

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.