Evidence map›Paper›PMID 41737559›Full record

ArticleFrontiers in pharmacology2026

Minnelide ameliorates Col4a5+/- mice by upregulating Col4a5 and alleviating endoplasmic reticulum stress.

Bao-Wei Ji, Jun-Chao Liu, Xue Wang, Ye Yin, Jing-Jia Zhang, Fu-Jie Wen, Hong Xu, Qian Shen, Jian Yu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Bao-Wei JiDepartment of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Jun-Chao LiuDepartment of Traditional Chinese Medicine, Children's Hospital of Fudan University, Shanghai, China.
Xue WangState Key Laboratory of Genetic Engineering and National Center for International Research of Development and Disease, Collaborative Innovation Center of Genetics and Development, Institute of Developmental Biology and Molecular Medicine, School of Life Sciences, Fudan University, Shanghai, China.
Ye YinDepartment of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Jing-Jia ZhangDepartment of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Fu-Jie WenPediatric Internal Medicine Department I, First People's Hospital of Kashi, Kashgar, Xinjiang, China.
Hong XuDepartment of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Qian ShenDepartment of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China.
Jian YuDepartment of Traditional Chinese Medicine, Children's Hospital of Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alport syndrome (AS) is a progressive hereditary nephropathy caused by mutations in collagen IV genes, notably COL4A5, leading to proteinuria and kidney failure. Current therapies using RAAS inhibitors show limited efficacy. Triptolide, the main active component of Objective: This study investigated the therapeutic potential and mechanisms of Minnelide in a female Col4a5 (X + X-) Alport syndrome mouse model. Methods: Mice were treated with Minnelide or vehicle for 3 months. Results: Minnelide significantly reduced proteinuria by 64.2%, improved glomerular pathology, upregulated renal Col4a5 expression, and suppressed endoplasmic reticulum (ER) stress. In podocytes, triptolide increased Col4a5 and alleviated ER stress. Col4a5 knockdown directly induced ER stress, which was reversed by triptolide treatment. Conclusion: Minnelide demonstrates potent renoprotective effects in AS by upregulating Col4a5 expression and mitigating podocyte ER stress, positioning it as a novel therapeutic candidate.

Indexed as

alport syndromeCo4a5endoplasmic reticulumminnelidepodocyte

Identifiers

PMID41737559
PMCPMC12926658

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.