Evidence map›Paper›PMID 41640280›Full record

ArticleActa biochimica et biophysica Sinica2026

Cardiac PTN-SIRT1 axis alleviates oxidative stress and promotes mitochondrial energy reprogramming to mitigate doxorubicin-induced cardiotoxicity through AMPK/PGC1α signaling.

Yuxiao Sun, Tianwen Wei, Hongping Xu, Hongda Li, Chang Zhou, Xianliang Liu, Yafei Li, Shangwei Huang, Qi Zhang, Xia Duan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Yuxiao SunDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Tianwen WeiDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Hongping XuDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Hongda LiDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Chang ZhouSchool of Medicine, Tongji University, Shanghai 200092, China.
Xianliang LiuSchool of Nursing and Health Sciences, Hong Kong Metropolitan University, Hong Kong SAR, China.
Yafei LiDepartment of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou 215000, China.
Shangwei HuangDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Qi ZhangDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Xia DuanNursing Department, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai 200092, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (DOX) remains a cornerstone chemotherapeutic agent for malignancies, yet its clinical utility is severely limited by dose-dependent cardiotoxicity, which can lead to progressive left ventricular dysfunction and heart failure. Pleiotrophin (PTN), a heparin-binding growth factor with diverse physiological functions, regulates glucose and lipid metabolism and promotes oxidative energy pathways. However, whether PTN exerts protective effects against DOX-induced cardiotoxicity (DIC) remains unclear. In this study, we establish cellular and animal models of DIC. DOX administration induces pronounced myocardial injury in both models, characterized by impaired ventricular contractility, increased fibrotic remodeling, and reduced cell viability. Concurrently, PTN protein expression is significantly downregulated in cardiomyocytes under DOX treatment. Overexpression of

Indexed as

AMP-Activated Protein KinasesCardiotoxicityCarrier ProteinsCytokinesDoxorubicinMitochondria, HeartOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSirtuin 1AnimalsEnergy MetabolismMaleMetabolic ReprogrammingMiceMyocytes, CardiacSignal TransductionAMP-Activated Protein KinasesCarrier ProteinsCytokinesDoxorubicinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphapleiotrophinPpargc1a protein, mouseSirt1 protein, mouseSirtuin 1doxorubicin-induced cardiotoxicitymitochondrial energy metabolismoxidative stresspleiotrophin

Identifiers

PMID41640280
PMCPMC12900733

What Socratic holds

Textmetadata
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.