The immune system accidentally targets the body's tissues, causing inflammation and tissue damage, the root causes of autoimmune illnesses. In recent studies, non-coding RNAs have been shown to significantly control gene expression and metabolic pathways linked to autoimmune diseases. This review investigates the effects of non-coding RNA on glucose metabolism, a route frequently dysregulated in autoimmune illnesses such as multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, and diabetes. We review how non-coding RNA affects immune cell activity modulation, glucose absorption, glycolysis, and other metabolic processes critical to immune function. We also investigate the possibility of using non-coding RNA-mediated metabolic pathway targeting as a new therapeutic approach to treat autoimmune disorders. By clarifying the complex interplay of non-coding RNA, glucose metabolism, and immune dysregulation, this study endeavors to enhance comprehension of autoimmune etiology and facilitate the creation of focused therapies.
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http://dx.doi.org/10.1016/j.humimm.2025.111269 | DOI Listing |
Anal Chim Acta
May 2025
Department of Human Sciences, The Ohio State University, USA; James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, 43210, USA. Electronic address:
Background: The imperative need for early cancer detection, which is crucial for improved survival rates in many severe cancers such as lung cancer, remains challenging due to the lack of reliable early-diagnosis technologies and robust biomarkers. To address this gap, innovative screening platforms are essential to unveil the chemical signatures of lung cancer and its treatments. It is established that the oxidative tumor environment induces alterations in host metabolic processes and influences endogenous volatile synthesis.
View Article and Find Full Text PDFCirc J
March 2025
Department of Cardiovascular Medicine, Shinshu University School of Medicine.
Background: The EMPA-REG OUTCOME trial confirmed empagliflozin reduced mortality and heart failure hospitalization risk. These findings raised the possibility that empagliflozin may modulate cardiac autonomic function in patients with type 2 diabetes (T2D).
Methods And Results: The EMPYREAN study was a prospective randomized open-label assessor-blinded multicenter investigation of patients with T2D without prior antidiabetic therapy with sodium-glucose cotransporter 2 or dipeptidyl peptidase 4 inhibitors.
Endocr J
March 2025
Department of Obstetrics and Gynecology, Ehime University Graduate School of Medicine, Ehime 791-0295, Japan.
The association between hypertensive disorders of pregnancy (HDP) and the subsequent development of type 2 diabetes (T2D) in Japanese general population remains unclear. To investigate the influence of HDP on long-term postpartum development of metabolic disorders and T2D, we conducted a population-based cross-sectional study using the 75 g oral glucose tolerance test (75g-OGTT) in 978 parous Japanese women (median age: 66 years). We further evaluated the combined effect of HDP and T2D susceptibility genes on developing T2D.
View Article and Find Full Text PDFBiol Pharm Bull
March 2025
Department of Pharmacy, College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyama-ku, Nagoya 463-8521, Japan.
We examined whether the glucose levels and awareness of individuals without diabetes changed after using a sensor-based intermittently scanned continuous glucose monitoring (isCGM) system in their daily lives. Japanese individuals without a diabetes diagnosis wore the isCGM system while maintaining a normal lifestyle during the baseline period. A certified diabetes educator coached them on how to improve their lifestyle based on information from sensor data, food journals, and body composition.
View Article and Find Full Text PDFFree Radic Biol Med
March 2025
Department of Radiation Oncology, Mays Cancer Center at UT Health San Antonio MD Anderson, Joe R. and Teresa Lozano Long School of Medicine, UT Health San Antonio, TX, USA; Barshop Institute for Longevity and Aging Studies at UT Health San Antonio, TX, USA. Electronic address:
Acetyl-CoA Synthetase Short Chain Family Member-1 (ACSS1) catalyzes the ligation of acetate and coenzyme A to generate acetyl-CoA in the mitochondria to produce ATP through the tricarboxylic acid (TCA) cycle. We recently generated an ACSS1-acetylation (Ac) mimic knock-in mouse, where lysine 635 was mutated to glutamine (K635Q), which structurally and biochemically mimics an acetylated lysine. ACSS1 enzymatic activity is regulated, at least in part, through the acetylation of lysine 635 in mice (lysine 642 in humans), a Sirtuin 3 deacetylation target.
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