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Pro-renin Receptor (PRR) as a Target to Reduce Non-alcoholic Fatty Liver Disease Post Liver Transplantation.
Curr Med Chem
January 2025
Transplant Research Center, Clinical Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Nonalcoholic fatty liver disease (NAFLD) is one of the main causes of chronic liver disorders following liver transplantation. The prorenin receptor (PRR) plays a role in glucose and lipid metabolism, and the hepatic dysregulation of PRR is associated with the upregulation of several molecular pathways, such as the mammalian target of rapamycin (mTOR) and Peroxisome proliferator-activated receptor (PPAR) that promotes hepatic lipogenesis and leads to lipid accumulation in hepatocytes by upregulation of lipogenic genes. PRR inhibition leads to a reduction in the hepatic expression of sortilin-1 and low-density lipoprotein receptor (LDLR) levels and down-regulation of pyruvate dehydrogenase (PDH) and acetyl-CoA carboxylase (ACC) and reduces fatty acids synthesis in hepatocytes.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
McGill University, Montreal, QC, Canada.
Background: Activation of the mTOR pathway is pivotal for microglia to induce and sustain neuroprotective functions (Ulland et al., 2017; Wang et al., 2022).
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Washington School of Medicine, Seattle, WA, USA.
Background: A drug cocktail targeting different processes of aging was tested in an aging mouse model of Alzheimer's disease (AD) neuropathologic change as an intervention to improve behaviors corresponding to cognitive dysfunction in AD.
Method: A cocktail of acarbose/rapamycin/phenylbutyrate or a control treatment was administered (medicated vs. non-medicated chow) chronically to 22 months-old mice that received viral vector injections to induce amyloid and tau pathology in the hippocampus at 24 months of age.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Pittsburgh, Pittsburgh, PA, USA.
Background: The bi-directional autophagy and inflammation network becomes progressively dysregulated with age, with systemic inflammation as a biomarker of this dysregulation including in Alzheimer's Disease (AD). We hypothesize that interventions which target the shared feature of systemic inflammation in the biology of aging and AD, via regulation of the autophagy-inflammation network, will prevent the conversion to disease pathogenesis in AD as well as improve healthspan and longevity in aging populations. While previous studies report benefits of mTOR inhibition including rapamycin in transgenic mouse models of familial AD, the present studies aim to evaluate this pathway in a model of sporadic, late onset AD (LOAD) and test the contribution of AMP-activated protein kinase (AMPK) as a critical regulator of the mTOR pathway.
View Article and Find Full Text PDFConstitutive activation of the Src-family kinases Fgr and Hck enhances the tumor burden of acute myeloid leukemia cells in immunocompromised mice.
Sci Rep
January 2025
Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Suite 523, Bridgeside Point II, 450 Technology Drive, Pittsburgh, PA, 15219, USA.
Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr.
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