ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Nuclear Autoantigenic Sperm Protein Promotes Cardiac Regeneration and Repair Through Activating the PDGFRB/AKT Pathway.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed.
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Nuclear Autoantigenic Sperm Protein Promotes Cardiac Regeneration and Repair Through Activating the PDGFRB/AKT Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Myocardial Infarction (MI) typically leads to unfavorable heart failure due to delayed reperfusion treatment. The adult heart is generally considered a nonregenerative organ. In contrast, the neonatal mammalian heart possesses the unique and transient ability to regenerate after injury. The underlying mechanisms governing heart regeneration remain largely unknown. Previous studies have shown that the nuclear auto-antigenic sperm protein (NASP) plays a crucial role in cell proliferation and tumorigenesis. This study explored the role of NASP in the heart for the first time, emphasizing its effect on cardiac regeneration and repair after injury. NASP exhibited high expression in neonatal myocardium and was observed to increase following apical resection (AR). The influence of NASP on cardiomyocyte proliferation was evaluated by examining cell cycle activity, mitosis, and cytokinesis staining using cardiomyocyte-specific overexpression or knockdown adenovirus 5 vectors. NASP knockdown inhibited heart regeneration in neonatal mice post-AR; whereas, NASP overexpression increased cardiomyocyte proliferation and promoted myocardial repair in adult mice post-MI. Mechanistically, NASP promoted cardiomyocyte proliferation through transcriptionally upregulating platelet-derived growth factor receptor beta (PDGFRB), subsequently activating the downstream AKT/c-MYC pathway. Our study highlights the key role of NASP in facilitating cardiac regenerative repair after injury, indicating its potential as a novel therapeutic target for MI.
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Registered trials
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.