ArticleNutrients2026
Exploring the Therapeutic Effect of
Article in Nutrients, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
BACKGROUND/
objectivesCardiac aging is characterized by increased oxidative stress and mitochondrial dysfunction in cardiomyocytes, leading to structural remodeling and functional decline.
methodsIn vitro, a cellular senescence model was established in H9c2 cardiomyocytes by D-gal induction to elucidate the effects of PCPs on senescence and mitochondrial dysfunction. In vivo, a mouse aging model was generated in C57BL/6J mice via continuous intraperitoneal injection of D-gal for three months to evaluate the ameliorative effects of PCPs on aging phenotypes and cardiac function.
resultsPCPs enhanced the antioxidant capacity of cardiomyocytes, improved energy metabolism homeostasis, maintained mitochondrial integrity, thereby synergistically regulating key aging-related signaling pathways such as suppressing overactivation of the p53/p21 axis and downregulating the expression of the senescence-associated secretory phenotype, thereby effectively mitigating myocardial injury and delaying cellular senescence.
conclusionsThis study demonstrates the anti-cardiac aging effects of PCPs at both cellular and animal levels, confirming that they protect cardiomyocytes by antagonizing oxidative stress, suppressing the p53/p21 pathway, and improving mitochondrial function. These findings provide an experimental basis for developing PCPs as a naturally sourced intervention against cardiac aging.
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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.