Evidence map›Paper›PMID 42234286›Full record

ArticleJournal of cardiovascular translational research2026

PSAP Protects Against Acute Myocardial Ischemia-Reperfusion Injury by Promoting ASAH1-Mediated Ceramide Metabolism.

Yiqing Chen, Xuan Ye, Chenyang Zha, Chi Jin, Huihua Chen, Hongyun Wang, Junjie Xiao

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 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

7 authors.

Yiqing ChenSchool of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Xuan YeSchool of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Chenyang ZhaInstitute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science, Shanghai University, Shanghai, 200444, China.
Chi JinInstitute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science, Shanghai University, Shanghai, 200444, China.
Huihua ChenSchool of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. chenhuihua@shutcm.edu.cn.
Hongyun WangInstitute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, Joint International Research Laboratory of Biomaterials and Biotechnology in Organ Repair (Ministry of Education), School of Life Science, Shanghai University, Shanghai, 200444, China. hongyun19@shu.edu.cn.
Junjie XiaoSchool of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. junjiexiao@live.cn.ORCID 0000-0002-9202-0003

Funding

National Natural Science Foundation of China 82370277
6 · The paper itself

Abstract

Myocardial ischemia-reperfusion (I/R) injury remains a leading cause of cardiovascular morbidity. However, due to the unclear underlying molecular mechanisms, effective therapeutic approaches are still lacking. This study aims to investigate the function and downstream mechanism of the lysosomal protein prosaposin (PSAP) in regulating ceramide homeostasis and cardiomyocyte apoptosis during acute I/R injury. In our study, we found that PSAP expression was significantly downregulated in the heart subjected to acute I/R surgery. Restoration of PSAP protein via AAV9-PSAP-OE in vivo significantly reduced infarct size and attenuated cardiomyocyte apoptosis. Similarly, PSAP overexpression in OGD/R-treated primary cardiomyocytes (NRCMs) decreased apoptosis, while PSAP knockdown exacerbated apoptosis. Mechanistically, PSAP accelerates the ceramide degradation pathway by rescuing the expression of the lysosomal N-acylsphingosine amidohydrolase 1 (ASAH1), thereby attenuating I/R-induced ceramide accumulation and cardiomyocyte apoptosis. Our results reveal a novel mechanism of PSAP function and highlight its potential as a therapeutic target for acute myocardial I/R injury.

Indexed as

Acid CeramidaseCeramidesMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacSaposinsAnimalsApoptosisCells, CulturedDisease Models, AnimalHumansMaleMice, Inbred C57BLRats, Sprague-DawleySignal TransductionAcid CeramidaseCeramidesPSAP protein, humanSaposinsApoptosisCeramideIschemia–Reperfusion InjuryPSAP

Identifiers

PMID42234286

What Socratic holds

Textmetadata
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.