Evidence map›Paper›PMID 40698245›Full record

ReviewFrontiers in endocrinology2025

Immune inflammation and metabolic interactions in the pathogenesis of diabetic nephropathy.

Guangjian Hou, Youzi Dong, Yuehua Jiang, Wenbo Zhao, Le Zhou, Shengnan Cao, Wei Li

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  7. CCL5 mRNA-enriched small extracellular vesicles from renal tubular epithelial cells enhance macrophage inflammatory responses in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  9. Mogroside V Alleviates Renal Injury in Diabetic Mice via Regulation of theInternational journal of molecular sciences · 2026
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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

7 authors.

Guangjian Hou *Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Youzi Dong *Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Yuehua JiangThe Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Wenbo ZhaoShandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Le ZhouThe Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Shengnan CaoShandong First Medical University (Shandong Academy of Medical Sciences), Jinan, Shandong, China.
Wei LiThe Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a significant microvascular complication of diabetes, substantially contributing to the global prevalence of end-stage renal disease. The pathogenesis of DN is multifactorial, involving both immune-inflammatory responses and metabolic dysregulation. Hyperglycemia, a hallmark of diabetes, initiates kidney damage through various mechanisms, including oxidative stress, the accumulation of advanced glycation end products (AGEs), and changes in renal blood flow. These processes lead to the hallmark pathological features of DN, such as glomerulosclerosis and tubulointerstitial fibrosis. The immune system, particularly macrophages, T cells, and B cells, plays a crucial role in the progression of kidney injury, with inflammatory cytokines such as TNF-α and IL-6 promoting renal inflammation and fibrosis. In addition, metabolic disturbances, notably insulin resistance and dysfunction in insulin signaling, contribute to kidney dysfunction through several key signaling pathways, including PI3K/Akt, mTOR, Wnt/β-catenin, JAK/STAT, and NF-κB. The interplay between immune responses and metabolic signaling exacerbates kidney damage, creating a feedback loop that accelerates the progression of DN. While current therapeutic strategies mainly focus on managing blood glucose levels and inflammation, emerging treatments, such as GLP-1 receptor agonists and SGLT2 inhibitors, show promise in addressing both the metabolic and inflammatory aspects of the disease. Future research should focus on unraveling the complex interactions between immune and metabolic pathways to develop more targeted and personalized treatments for DN. This review highlights the significance of these mechanisms in the pathophysiology of DN and calls for innovative therapeutic approaches to combat this debilitating condition.

Indexed as

Diabetic NephropathiesInflammationAnimalsHumansInsulin ResistanceOxidative StressSignal Transductiondiabetic nephropathyimmune cellsimmune-inflammatory responsekidney damagemetabolic signaling pathways

Identifiers

PMID40698245
PMCPMC12279506

What Socratic holds

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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 Socratic graph.