Simmaron Research

Excited to announce that Simmaron Research has received a new NIH grant to advance our research into understanding the role of mTOR activation in the pathogenesis of ME/CFS. This award represents an important milestone in our efforts to unravel the underlying molecular mechanisms of this complex and debilitating disease and identify potential new therapeutic targets. We are grateful to everyone who has contributed to making this research possible and look forward to the discoveries ahead! Explore the grant on NIH RePORTER: reporter.nih.gov/project-det…

Rapamycin may tie these three converging threads together in ME/CFS. @RedefiningMECFS @UWM @SpringerNature @ggottschalkPhD The link of our newest article link.springer.com/article/10…

Our lab @RedefiningMECFS is a part of drug discovery consortium with MIDD @UWM. A collaborative research (Redox Biology; IF 11.9) identified a novel boronated prodrug that kills TNBC tumor cells by augmenting the production of reactive oxygen species. sciencedirect.com/science/ar…

Our team @RedefiningMECFS @ggottschalkPhD continues to perform ground-breaking research in decoding the role of ATG13 in chronic inflammation and now our new research (Toriola M et.al.) is now published in @SpringerNature’s Q1 immunology journal Inflammation Research. doi.org/10.1007/s00011-025-0…  Background: CD40 is a key surface antigen expressed on macrophages and other myeloid cells, where it plays a central role in innate immunity by sustaining their inflammatory phenotype. In our earlier study (Immunologic Res 2025) , we demonstrated that the impaired autophagy can trigger sub-threshold infiltration of CD40-immunoreactive macrophages into the vasculature of skeletal muscle tissue. This infiltration contributes to chronic inflammatory changes affecting muscle-serving nerve fibers. Findings: In our current work, we delineate the underlying mechanism. We demonstrate that the genetic depletion of atg13 gene and the subsequent autophagy impairment may initiate a series of metabolic changes in myeloid cells. These changes start with the deficit in mitochondrial energy metabolism (confirmed by Seahorse analyses of OXPHOS and glycolysis), then the augmentation of reactive oxygen species ( Mito-ROS assay), then the nifrosylative inactivation of cellular deacetylase enzyme called SIRT1 , which maintains the acetylation status of NF-κB. These series of metabolic changes drive the induction of the inflammatory phenotype in perivascular macrophages. Along with CD40, we examined the impact of atg13-dependent autophagy impairment in the expressions of other surface antigens such as CD86, CD163, and CD206 in the context of inflammatory response in myeloid cells. Summary: The pathway we describe highlights how NF-kB-mediated inflammatory changes in myeloid cells may contribute to the neurogenic symptoms of muscle fatigue, post-exertional malaise, and potentially post-infectious fatigue syndromes. @MECFSNews @UWM

Simmaron @RedefiningMECFS @ggottschalkPhD is excited for the early preclinical results of our small molecule-inhibitors SIMMPYRA-1 and 2 to modulate STAT signaling events in reducing chronic inflammation associated with mononucleosis and cytokine upregulations.@BCRFcure @PlzSolveCFS