Evidence mapPaperPMID 38498274Full record

ReviewInternational urology and nephrology2024

The role of PI3K/Akt signaling pathway in chronic kidney disease.

Hongshuang Wang, Lanjun Gao, Chenchen Zhao, Fang Fang, Jiazhi Liu, Zheng Wang, Yan Zhong, Xiangting Wang

Abstract readReview
PubMed Publisher
In one paragraph

Review in International urology and nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
15.2field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 63 citations in OpenAlex.

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  14. Telomere Dysfunction in Renal Tubular Epithelial Cells Leads to Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025
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  19. Systems Pharmacology and Multi-Omics Elucidation ofPharmaceuticals (Basel, Switzerland) · 2025
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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 1 institution in 1 country.

Hongshuang Wang *Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Lanjun Gao *Graduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Chenchen ZhaoGraduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Fang FangGraduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Jiazhi LiuGraduate School, Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Zheng WangHebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns Research, Shijiazhuang, 050091, China.
Yan ZhongHebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns Research, Shijiazhuang, 050091, China. zy1987821@hebcm.edu.cn.
Xiangting WangHebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns Research, Shijiazhuang, 050091, China. wangxiangting@hebcm.edu.cn.
Hebei University of Chinese Medicine · CN

Funding

Natural Science Foundation of Hebei Province H2022423351
6 · The paper itself

Abstract

Chronic kidney disease (CKD), including chronic glomerulonephritis, IgA nephropathy and diabetic nephropathy, are common chronic diseases characterized by structural damage and functional decline of the kidneys. The current treatment of CKD is symptom relief. Several studies have reported that the phosphatidylinositol 3 kinases (PI3K)/protein kinase B (Akt) signaling pathway is a pathway closely related to the pathological process of CKD. It can ameliorate kidney damage by inhibiting this signal pathway which is involved with inflammation, oxidative stress, cell apoptosis, epithelial mesenchymal transformation (EMT) and autophagy. This review highlights the role of activating or inhibiting the PI3K/Akt signaling pathway in CKD-induced inflammatory response, apoptosis, autophagy and EMT. We also summarize the latest evidence on treating CKD by targeting the PI3K/Akt pathway, discuss the shortcomings and deficiencies of PI3K/Akt research in the field of CKD, and identify potential challenges in developing these clinical therapeutic CKD strategies, and provide appropriate solutions.

Indexed as

Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRenal Insufficiency, ChronicSignal TransductionApoptosisAutophagyEpithelial-Mesenchymal TransitionHumansOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktChronic kidney diseaseMechanismPI3K/AktTherapeutic target

Identifiers

PMID38498274
OpenAlexW4392907455

What Socratic 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 Socratic graph.