ArticleParasites & vectors2025
PD-1-dependent therapeutic effect of Trichinella spiralis cystatin on myocardial infarction in a mice model.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- The critical window for host defense: macrophage trogocytosis eliminatesFrontiers in immunology · 2026Article
- The role of the PD-1/PD-L1 immune checkpoint pathway in myocardial infarction: a review from pathophysiological mechanisms to therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
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Authors and funding
13 authors.
Funding
Abstract
backgroundIschemia-induced inflammation is the primary pathological mechanism underlying cardiac tissue injury caused by myocardial infarction (MI). Trichinella spiralis cystatin (Ts-Cys) has been shown to regulate macrophage polarization and alleviate various inflammatory and immune-related diseases. Programmed cell death-1 (PD-1) is a crucial checkpoint receptor molecule and highly involved in maintaining immune tolerance. In this study, our aims were to investigate whether recombinant Ts-Cys protein (rTs-Cys) could be used to treat MI with recruited macrophage-dominant myocardial inflammation and whether PD-1 is involved in the immunomodulation of Ts-Cys in inflammatory diseases.
methodsMI models were established in wild-type (WT) and PD-1 knockout (PD-1
resultsIn WT mice, rTs-Cys treatment significantly improved the 28-day survival rate and cardiac function, reduced local inflammatory cell infiltration and cardiac pathological damage and increased VEGF expression levels of MI mice. The therapeutic effect of rTs-Cys was associated with macrophage polarization from the pro-inflammatory M1 phenotype to the regulatory M2 phenotype with reduced levels of inflammatory cytokines (TNF-α and IL-6) and increased levels of regulatory cytokines (IL-10 and TGF-β), as determined by both in vivo and in vitro tests. However, this therapeutic effect of rTs-Cys on MI was significantly reduced in PD-1
conclusionsrTs-Cys promotes M2-type polarization of macrophages through the PD-1 pathway to alleviate MI in mice and is, therefore, a potential drug for the treatment of MI and other inflammation-related diseases with involvement of the PD-1 checkpoint molecule.
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