Evidence map›Paper›PMID 39247486›Full record

ReviewJournal of pharmaceutical analysis2024

Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis.

Yini Bao, Qiyuan Shan, Keda Lu, Qiao Yang, Ying Liang, Haodan Kuang, Lu Wang, Min Hao, Mengyun Peng, Shuosheng Zhang and 1 more

Abstract readReview
In one paragraph

Review in Journal of pharmaceutical analysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Review
  5. Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Targeting renal tubular epithelial cellsActa pharmaceutica Sinica. B · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  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

11 authors.

Yini BaoSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Qiyuan ShanSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Keda LuThe Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310009, China.
Qiao YangSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Ying LiangSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Haodan KuangSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Lu WangSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Min HaoSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Mengyun PengSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Shuosheng ZhangCollege of Chinese Materia Medica and Food Engineering, Shanxi University of Chinese Medicine, Jinzhong, Shanxi, 030600, China.
Gang CaoSchool of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, 310053, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is a devastating consequence of progressive chronic kidney disease, representing a major public health challenge worldwide. The underlying mechanisms in the pathogenesis of renal fibrosis remain unclear, and effective treatments are still lacking. Renal tubular epithelial cells (RTECs) maintain kidney function, and their dysfunction has emerged as a critical contributor to renal fibrosis. Cellular quality control comprises several components, including telomere homeostasis, ubiquitin-proteasome system (UPS), autophagy, mitochondrial homeostasis (mitophagy and mitochondrial metabolism), endoplasmic reticulum (ER, unfolded protein response), and lysosomes. Failures in the cellular quality control of RTECs, including DNA, protein, and organelle damage, exert profibrotic functions by leading to senescence, defective autophagy, ER stress, mitochondrial and lysosomal dysfunction, apoptosis, fibroblast activation, and immune cell recruitment. In this review, we summarize recent advances in understanding the role of quality control components and intercellular crosstalk networks in RTECs, within the context of renal fibrosis.

Indexed as

AutophagyMitochondriaQuality controlRenal fibrosisRenal tubular epithelial cellsTelomere homeostasis

Identifiers

PMID39247486
PMCPMC11377145

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.