Evidence map›Paper›PMID 36091814›Full record

ReviewFrontiers in pharmacology2022

The critical role of dysregulated autophagy in the progression of diabetic kidney disease.

Ziwei Zhang, Yuting Sun, Jiaojiao Xue, De Jin, Xiangyan Li, Daqing Zhao, Fengmei Lian, Wenxiu Qi, Xiaolin Tong

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Integrated multiomic analyses: An approach to improve understanding of diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023
    Review
  11. 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

9 authors at 4 institutions in 1 country.

Ziwei ZhangCollege of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
Yuting SunDepartment of Endocrinology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Jiaojiao XueCollege of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
De JinHangzhou Hospital of Traditional Chinese Medicine, Hangzhou, China.
Xiangyan LiNortheast Asia Research Institute of Traditional Chinese Medicine, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
Daqing ZhaoNortheast Asia Research Institute of Traditional Chinese Medicine, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
Fengmei LianGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Wenxiu QiNortheast Asia Research Institute of Traditional Chinese Medicine, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Biomacromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.
Xiaolin TongInstitute of Metabolic Diseases, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Changchun University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNGuang’anmen Hospital · CNHangzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is one of the major public health problems in society today. It is a renal complication caused by diabetes mellitus with predominantly microangiopathy and is a major cause of end-stage renal disease (ESRD). Autophagy is a metabolic pathway for the intracellular degradation of cytoplasmic products and damaged organelles and plays a vital role in maintaining homeostasis and function of the renal cells. The dysregulation of autophagy in the hyperglycaemic state of diabetes mellitus can lead to the progression of DKD, and the activation or restoration of autophagy through drugs is beneficial to the recovery of renal function. This review summarizes the physiological process of autophagy, illustrates the close link between DKD and autophagy, and discusses the effects of drugs on autophagy and the signaling pathways involved from the perspective of podocytes, renal tubular epithelial cells, and mesangial cells, in the hope that this will be useful for clinical treatment.

Indexed as

autophagosomeautophagydiabetic kidney diseaselysosomepodocytesrenal tubular epithelial cells

Identifiers

PMID36091814
PMCPMC9453227
OpenAlexW4293036717

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.