Evidence map›Paper›PMID 40226441›Full record

ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2025

Diabetic Kidney Disease: Disease Progression Driven by Positive Feedback Loops and Therapeutic Strategies Targeting Pathogenic Pathways.

Gaozhi P Mo, Yao Zhu, Yue You, Hui Chen, Jiahao Zhang, Bunhav Ku, Haichuan Yu, Zhiyong Peng

Abstract readReview
In one paragraph

Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Frontiers in pharmacology · 2026
    Article
  3. 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.

Gaozhi P Mo *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Yao Zhu *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Yue YouDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Hui ChenDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Jiahao ZhangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Bunhav KuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.
Haichuan YuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.ORCID 0000-0002-4231-2542
Zhiyong PengDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a major complication of diabetes mellitus, with its pathogenesis intricately regulated by dynamic feedback mechanisms. This comprehensive review systematically analyzes the hierarchical feedback networks driving DKD progression, spanning from systemic interactions to molecular cross-talks. We reveal that self-amplifying positive feedback loops dominate the disease process, manifested through three key dimensions: (1) The systemic triad of hyperglycemia-hypertension-proteinuria establishes a vicious cycle accelerating renal dysfunction; (2) Cellular homeostasis collapse through cross-amplified cell death modalities (apoptosis, pyroptosis, ferroptosis) and cell cycle dysregulation; (3) Molecular cascades centered on AGE/RAGE signaling that fuel chronic inflammation and fibrotic transformation. Collectively, these form a major positive feedback loop where PKC activation, oxidative stress propagation, and TGF-β-mediated fibrosis induced by hyperglycemia lead to progressive renal deterioration and fibrosis. Therapeutically, we propose a dual intervention strategy targeting both the acute phase through AGE/RAGE axis inhibition, coupled with chronic phase via precision modulation of fibrotic pathways. These findings redefine DKD progression as a self-reinforcing network disorder, providing a roadmap for developing multi-target therapies that disrupt pathological feedback loops while preserving renal repair mechanisms.

Indexed as

advanced glycation end productsdiabetic kidney diseasefeedbackfibrosishyperglycemiatreatment

Identifiers

PMID40226441
PMCPMC11994106

What OpenQuestion holds

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LicenceCC BY-NC
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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.