Evidence map›Paper›PMID 39707216›Full record

ReviewMolecular medicine (Cambridge, Mass.)2024

Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.

Fengzhao Liu, Zhenyu Yang, Jixin Li, Tao Wu, Xiangyu Li, Lijuan Zhao, Wenru Wang, Wenfei Yu, Guangheng Zhang, Yunsheng Xu

Abstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

10 authors.

Fengzhao Liu *First College of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.
Zhenyu Yang *Graduate School of Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Jixin Li *Xi Yuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Tao WuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 100029, China.
Xiangyu LiWangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, 100102, China.
Lijuan ZhaoFirst College of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.
Wenru WangXi Yuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Wenfei YuFirst College of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.
Guangheng ZhangFirst College of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, 250014, China.
Yunsheng XuDepartment of Endocrinology, Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250001, China. xyslaoshi@163.com.

Funding

National Key Research and Development Program of China 2023YFC3606200Taishan Scholar Project of Shandong Province ts201712097
6 · The paper itself

Abstract

Diabetic kidney disease (DKD), one of the most prevalent microvascular complications of diabetes, arises from dysregulated glucose and lipid metabolism induced by hyperglycemia, resulting in the deterioration of renal cells such as podocytes and tubular epithelial cells. Programmed cell death (PCD), comprising apoptosis, autophagy, ferroptosis, pyroptosis, and necroptosis, represents a spectrum of cell demise processes intricately governed by genetic mechanisms in vivo. Under physiological conditions, PCD facilitates the turnover of cellular populations and serves as a protective mechanism to eliminate impaired podocytes or tubular epithelial cells, thereby preserving renal tissue homeostasis amidst hyperglycemic stress. However, existing research predominantly elucidates individual modes of cell death, neglecting the intricate interplay and mutual modulation observed among various forms of PCD. In this comprehensive review, we delineate the diverse regulatory mechanisms governing PCD and elucidate the intricate crosstalk dynamics among distinct PCD pathways. Furthermore, we review recent advancements in understanding the pathogenesis of PCD and explore their implications in DKD. Additionally, we explore the potential of natural products derived primarily from botanical sources as therapeutic agents, highlighting their multifaceted effects on modulating PCD crosstalk, thereby proposing novel strategies for DKD treatment.

Indexed as

Diabetic NephropathiesRegulated Cell DeathAnimalsApoptosisAutophagyHumansSignal TransductionDiabetic kidney diseaseNatural productsPodocytesProgrammed cell deathTubular epithelial cells

Identifiers

PMID39707216
PMCPMC11660506

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.