Evidence mapPaperPMID 41113404Full record

ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025

Targeted Delivery of Triptolide Alleviates Diabetic Nephropathy via Inactivation of JAK2-STAT1 Signaling.

Rongshuang Huang, Xinrui Li, Fan Guo, Yanping Li, Liang Ma, Ping Fu

Abstract read
In one paragraph

Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

  1. Article
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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

6 authors.

Rongshuang HuangDepartment of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.
Xinrui LiDepartment of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.
Fan GuoDepartment of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.
Yanping LiDepartment of Pharmacy, Institute of Metabolic Diseases and Pharmacotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Liang MaDepartment of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.
Ping FuDepartment of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu 610041, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Inflammation and fibrosis are key features of diabetic nephropathy (DN). Triptolide (TP) exhibits anti-inflammatory and anti-fibrotic properties, though its mechanisms of action in DN remain unclear. CREKA (Cys-Arg-Glu-Lys-Ala) is a pentapeptide that specifically binds to fibronectin (FN), and the CREKA-modified liposome (CREKA-Lip) represents a novel FN-targeted drug delivery system. This study aimed to investigate the role of TP in diabetic db/db mice and determine whether encapsulation within CREKA-Lip enhances therapeutic efficacy while reducing the multi-organ toxicity of TP. Methods: Eight-week-old diabetic db/db mice received tail vein injections twice weekly with vehicle, free TP, or CREKA-Lip/TP for 10 weeks. Urine and serum parameters were measured, and kidney, heart, liver, and testis tissues were collected for pathological evaluation. Protein-protein interaction networks were constructed using Cytoscape and its plug-ins to identify core targets and elucidate the therapeutic mechanism of TP against DN. Inflammatory, fibrotic, apoptotic, and lipid metabolism markers were evaluated in the kidneys of diabetic mice with DN and in high glucose-treated mouse mesangial cells and podocytes using qPCR, Western blot, immunohistochemistry, and immunofluorescence assays. Results: TP administration reduced fasting blood glucose levels and glomerular mesangial expansion in diabetic mice. TP significantly suppressed renal inflammation, fibrosis, and apoptosis while enhancing lipid metabolism. Integration of network pharmacology, molecular docking, and transcriptomics revealed that TP ameliorated DN by inhibiting the JAK2-STAT1 signaling pathway. Conclusion: TP improves renal inflammation, fibrosis, apoptosis, and lipid homeostasis, thereby ameliorating DN by inhibiting JAK2-STAT1 activation. Targeted delivery of TP via FN-binding CREKA-Lip enhances therapeutic efficacy while minimizing multi-organ toxicity.

Indexed as

Diabetic NephropathiesDiterpenesJanus Kinase 2PhenanthrenesSignal TransductionSTAT1 Transcription FactorAnimalsDiabetes Mellitus, ExperimentalDrug Delivery SystemsEpoxy CompoundsMaleMiceMice, Inbred C57BLDiterpenesEpoxy CompoundsJak2 protein, mouseJanus Kinase 2PhenanthrenesStat1 protein, mouseSTAT1 Transcription FactortriptolideDiabetic nephropathyPolypeptide-liposomeSTAT1ToxicityTriptolide

Identifiers

PMID41113404
PMCPMC12531011

What Socratic holds

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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.