ArticleFrontiers in pharmacology2026
CCR2
Article in Frontiers in pharmacology, 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: Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, with exercise emerging as a potential non-pharmacological strategy to reduce adverse outcomes. Prior studies examining macrophage responses to exercise primarily focused on recruited C-C motif chemokine receptor 2 (CCR2 Objectives: To determine the role of CCR2 Methods: We validated a voluntary exercise wheel-running model with diphtheria toxin mediated depletion of CCR2 Results: Echocardiography revealed voluntary exercise increased left ventricle (LV) mass and wall thickness while preserving cardiac function compared to sedentary conditions. Exercise increased morphometric heart, LV, and right ventricle (RV) mass as well as Fulton index. Cardiomyocyte cross-sectional area was also increased in both the LV and RV of voluntary exercise mice. Cardiac remodeling occurred in both sexes, with sex-specific differences in the LV. Immunofluorescence quantification of interstitial CD68 Conclusion: Together, these findings identify CCR2
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