Peroxisomes play a central role in human health and have biochemical properties that promote their use in many biotechnology settings. With a primary role in lipid metabolism, peroxisomes share a niche with lipid droplets within the endomembrane-secretory system. Notably, factors in the ER required for the biogenesis of peroxisomes also impact the formation of lipid droplets. The dynamic interface between peroxisomes and lipid droplets, and also between these organelles and the ER and mitochondria, controls their metabolic flux and their dynamics. Here, we review our understanding of peroxisome biogenesis to propose and reframe models for understanding how peroxisomes are formed in cells. To more fully understand the roles of peroxisomes and to take advantage of their many properties that may prove useful in novel therapeutics or biotechnology applications, we recast mechanisms controlling peroxisome biogenesis in a framework that integrates inference from these models with experimental data.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054992 | PMC |
http://dx.doi.org/10.1083/jcb.201912100 | DOI Listing |
Microglia modulate their cell state in response to various stimuli. Changes to cellular lipids often accompany shifts in microglial cell state, but the functional significance of these metabolic changes remains poorly understood. In human induced pluripotent stem cell-derived microglia, we observed that both extrinsic activation (by lipopolysaccharide treatment) and intrinsic triggers (the Alzheimer's disease-associated genotype) result in accumulation of triglyceride-rich lipid droplets.
View Article and Find Full Text PDFWhile fructose is a key dietary component, concerns have been raised about its potential risks to the liver. This study aimed to assess quercetin's protective effects against fructose-induced mouse hepatic steatosis. Thirty-two male C57BL/6J mice were randomly allocated into four groups: control, high fructose diet (HFrD), HFrD supplemented with low-dose quercetin (HFrD+LQ), and HFrD supplemented with high-dose quercetin (HFrD+HQ).
View Article and Find Full Text PDFFood Sci Nutr
January 2025
Laboratory of Biotechnology and Natural Resources Valorization, Faculty of Sciences Ibn Zohr University Agadir Morocco.
Hepatic steatosis/non-alcoholic fatty liver disease is a major public health delinquent caused by the excess deposition of lipid into lipid droplets (LDs) as well as metabolic dysregulation. Hepatic cells buildup with more fat molecules when a person takes high fat diet that is excessive than the body can handle. At present, millions of people in the world are affected by this problem.
View Article and Find Full Text PDFJHEP Rep
January 2025
Department of Microbiology and Immunology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Background & Aims: Hepatic steatosis, characterized by lipid accumulation in hepatocytes, is a key diagnostic feature in patients with chronic hepatitis C virus (HCV) infection. This study aimed to clarify the involvement of phospholipid metabolic pathways in the pathogenesis of HCV-induced steatosis.
Methods: The expression and distribution of lipid species in the livers of human liver chimeric mice were analyzed using imaging mass spectrometry.
Arthritis Rheumatol
January 2025
Department of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, 55905, USA.
Rheumatoid arthritis (RA) is a life-long autoimmune disease caused by the confluence of genetic and environmental variables that lead to loss of self-tolerance and persistent joint inflammation. RA occurs at the highest incidence in individuals >65 years old, implicating the aging process in disease susceptibility. Transformative approaches in molecular immunology and in functional genomics have paved the way for pathway paradigms underlying the replacement of immune homeostasis with auto-destructive immunity in affected patients, including the process of immune aging.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!