Evidence map›Paper›PMID 40067577›Full record

ArticleInflammation2025

Canagliflozin Attenuates Podocyte Inflammatory Injury through Suppressing the TXNIP/NLRP3 Signaling Pathway in Diabetic Kidney Disease Mice.

Siyu Li, Jie Wang, Ying Chen, Yanlu Cheng, Yanan Wang, Nuowen Xu, Hao Wang, Li Wang, Yangfeng Chi, Xiaoxue Ye and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
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

17 authors.

Siyu Li *Shanghai Putuo Central School of Clinical Medicine, Department of Integrated Traditional Chinese and Western Medicine, Anhui Medical University, Shanghai, 200062, China.
Jie Wang *Department of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Ying Chen *Department of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Yanlu ChengDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Yanan WangDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Nuowen XuDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Hao WangDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Li WangShanghai Putuo Central School of Clinical Medicine, Department of Integrated Traditional Chinese and Western Medicine, Anhui Medical University, Shanghai, 200062, China.
Yangfeng ChiDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Xiaoxue YeDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Yanting ShiDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Ji FangDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Xingmei YaoDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Jiebo HuangDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China.
Qing XiaCommunity Health Service Center of Caoyang Street, Putuo District, Shanghai, 200062, China.
Tianli BaiDepartment of Nephrology, Laboratory of Renal Disease, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, 164 LanXi Road, Shanghai, 200062, China. 348875870@163.com.
Bingbing ZhuShanghai Putuo Central School of Clinical Medicine, Department of Integrated Traditional Chinese and Western Medicine, Anhui Medical University, Shanghai, 200062, China. bingbingzhu630@sina.cn.

Funding

Clinical specialty of Shanghai Putuo District Health System project 2021tszk02Key Medical Discipline Project of Shanghai Municipal Health Bureau ZK2019A12Putuo District of shanghai Science and Technology Commission Research Project ptkwws202311Traditional Chinese Medicine Research Project of Shanghai Municipal Health Commission 2024QN080
6 · The paper itself

Abstract

Diabetic kidney disease (DKD), a leading cause of end-stage renal disease (ESRD), poses a serious threat to global health. Aseptic inflammation and pyroptosis of podocytes are crucial factors contributing to the pathogenesis and progression of DKD. Sodium-glucose cotransporter 2 inhibitors (SGLT2i), a novel class of antidiabetic agents widely used in clinical settings, may exert a protective effect on podocyte injury, although the underlying mechanisms remain poorly understood. This study uses the streptozotocin (STZ) -induced DKD mouse model to further explore the mechanism by which SGLT2i protect podocytes. The results demonstrated that Canagliflozin (CANA) treatment significantly improved serum creatinine levels, 24-h urinary albumin excretion, and urinary albumin-to-creatinine ratio (UACR) in DKD mice. Additionally, CANA treatment attenuated glomerular and podocyte injury, reducing overall pathological damage. Mechanistically, CANA reduced the expression of key inflammatory markers in the renal cortex of DKD mice, including TXNIP, NLRP3, ASC, caspase-1, IL-1β, IL-18, and GSDMD. These findings suggest that CANA may be an effective therapeutic agent for DKD by inhibiting the TXNIP-NLRP3 inflammasome pathway and preventing podocyte pyroptosis.

Indexed as

CanagliflozinCarrier ProteinsDiabetic NephropathiesNLR Family, Pyrin Domain-Containing 3 ProteinPodocytesSodium-Glucose Transporter 2 InhibitorsAnimalsDiabetes Mellitus, ExperimentalInflammasomesInflammationMaleMicePyroptosisSignal TransductionThioredoxinsCanagliflozinCarrier ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseSodium-Glucose Transporter 2 InhibitorsThioredoxinsTxnip protein, mouseCanagliflozinDiabetic kidney diseaseInflammationNucleotide binding oligomerization domain-like receptors 3

Identifiers

PMID40067577
PMCPMC12596306

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.