Evidence map›Paper›PMID 42464669›Full record

ArticleMolecular medicine reports2026

PCSK9 alleviates doxorubicin‑induced pyroptosis of cardiomyocytes.

Chaochu Cui, Jinyu Zhao, Xiaoqian Li, Shengming Huang, Gang Liu, Xinhui Xu, Can Guo, Tiesuo Zhao, Jiang Du, Shipeng Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 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

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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

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

12 authors.

Chaochu Cui *Henan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Jinyu Zhao *Henan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Xiaoqian LiHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Shengming HuangHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Gang LiuHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Xinhui XuHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Can GuoHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Tiesuo ZhaoDepartment of Immunology, School of Basic Medical Sciences, Henan Medical University, Xinxiang, Henan 453000, P.R. China.
Jiang DuHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Shipeng LiHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Xianwei WangHenan Key Laboratory of Medical Tissue Regeneration, Henan Medical University, Xinxiang, Henan 453003, P.R. China.
Jianbo YangTeaching Laboratory of Medical Imaging Technology, School of Life Sciences and Technology, Henan Medical University, Xinxiang, Henan 453003, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolonged survival of patients with cancer has increased the need to address chemotherapy‑related cardiovascular complications. Doxorubicin (DOX), a widely used anthracycline, is associated with dose‑dependent cardiotoxicity, known as DOX‑induced cardiotoxicity (DIC), which limits its clinical utility. DOX triggers cardiomyocyte pyroptosis via the NLRP3/caspase‑1/gasdermin D pathway, a potential underlying mechanism of DIC. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a key regulator of lipid metabolism and inflammation, has been implicated in NLRP3 inflammasome activation and the progression of cardiovascular diseases; however, its role in DIC remains unclear. The present study demonstrated that DOX downregulates PCSK9 expression in cardiomyocytes in a dose‑dependent manner. Through proteomic analysis and PCSK9 knockout cell and mouse models, it was found that the deletion of PCSK9 exacerbated DOX‑induced pyroptosis and cardiac dysfunction. These results revealed the protective effect of PCSK9 in DOX‑mediated cardiotoxicity and indicated that PCSK9 regulation may provide a new cardioprotective strategy for patients receiving anthracycline chemotherapy.

Indexed as

DoxorubicinMyocytes, CardiacProprotein Convertase 9PyroptosisAnimalsAntibiotics, AntineoplasticCardiotoxicityHumansMaleMiceMice, KnockoutAntibiotics, AntineoplasticDoxorubicinPcsk9 protein, mouseProprotein Convertase 9cancercardiotoxicitydoxorubicinproprotein convertase subtilisin/kexin type 9pyroptosis

Identifiers

PMID42464669
PMCPMC13396902

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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 OpenQuestion graph.