Evidence map›Paper›PMID 32583573›Full record

ReviewJournal of cellular and molecular medicine2020

Lysosomal dysfunction-induced autophagic stress in diabetic kidney disease.

Hui Juan Zheng, Xueqin Zhang, Jing Guo, Wenting Zhang, Sinan Ai, Fan Zhang, Yaoxian Wang, Wei Jing Liu

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.5field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Telomeric autophagy in human health, aging, and diseases.Frontiers in molecular biosciences · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Novel Insights into Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  16. Review
  17. Article
  18. Role of autophagy in angiogenic potential of vascular pericytes.Frontiers in cell and developmental biology · 2024
    Review
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Hui Juan ZhengRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-8394-0844
Xueqin ZhangRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-1803-7341
Jing GuoRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-4781-8200
Wenting ZhangRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.
Sinan AiRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.
Fan ZhangRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.
Yaoxian WangRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-1927-9529
Wei Jing LiuRenal Research Institution of Beijing University of Chinese Medicine, Beijing, China.ORCID 0000-0002-5356-7057
Beijing University of Chinese Medicine · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The catabolic process that delivers cytoplasmic constituents to the lysosome for degradation, known as autophagy, is thought to act as a cytoprotective mechanism in response to stress or as a pathogenic process contributing towards cell death. Animal and human studies have shown that autophagy is substantially dysregulated in renal cells in diabetes, suggesting that activating autophagy could be a therapeutic intervention. However, under prolonged hyperglycaemia with impaired lysosome function, increased autophagy induction that exceeds the degradative capacity in cells could contribute toward autophagic stress or even the stagnation of autophagy, leading to renal cytotoxicity. Since lysosomal function is likely key to linking the dual cytoprotective and cytotoxic actions of autophagy, it is important to develop novel pharmacological agents that improve lysosomal function and restore autophagic flux. In this review, we first provide an overview of the autophagic-lysosomal pathway, particularly focusing on stages of lysosomal degradation during autophagy. Then, we discuss the role of adaptive autophagy and autophagic stress based on lysosomal function. More importantly, we focus on the role of autophagic stress induced by lysosomal dysfunction according to the pathogenic factors (including high glucose, advanced glycation end products (AGEs), urinary protein, excessive reactive oxygen species (ROS) and lipid overload) in diabetic kidney disease (DKD), respectively. Finally, therapeutic possibilities aimed at lysosomal restoration in DKD are introduced.

Indexed as

AnimalsAutophagyDiabetes MellitusDiabetic NephropathiesHumansKidneyLysosomesReactive Oxygen SpeciesReactive Oxygen Speciesautophagic stressautophagydiabetic kidney diseaselysosomal dysfunction

Identifiers

PMID32583573
PMCPMC7412686
OpenAlexW3038033037

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.