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SLC15A4 mediates M1-prone metabolic shifts in macrophages and guards immune cells from metabolic stress

Acknowledgments This work was supported by NIH grant DK45334 Footnotes Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication

Thus, it seems like a no brainer if we employ methods which will increase the expression of genes that are involved in oxidative stress resistance, particularly oxidative damage, we may get the benefits of IGF-1 without the fall off in longevity

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Our team has found that this approach can yield results in research settings that far surpass what either compound could achieve on its own