The maintenance of the functional potential of mitochondria is directly related to epigenetic factors, microRNAs (miRs), and mitomicroRNAs (mitomiRs). An important role in the development of metabolic syndrome (MetS)/obesity is attributed to miRs, which have pro-inflammatory or anti-inflammatory potential and can penetrate the mitochondrial matrix. Deciphering the mechanisms responsible for the transport of miRs into the mitochondria would, we believe, allow us to use the knowledge obtained to build designs for the transport of drugs/mitomiRs into cells/mitochondria with low toxicity. A thorough understanding of the polyfunctionality/versatility of individual mitomiRs in specific cells (cell cultures, tissues: adipocytes, brain cells) will allow targeting cellular metabolism to comprehensively block the central link in disease pathogenesis with low potential side effects of this treatment. In this review, we have attempted to identify the key miRs/mitomiRs associated with MetS that affect mitochondrial function. In our opinion, further research should focus specifically on the miR/mitomiRs described here and further investigate their potential in the development of MetS and its components.
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http://dx.doi.org/10.2174/0109298673361354250224060829 | DOI Listing |
Nanomaterials (Basel)
February 2025
School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
Acute myocardial infarction, a leading cause of death globally, is often associated with cardiometabolic disorders such as atherosclerosis and metabolic syndrome. Metabolic treatment of these disorders can improve cardiac outcomes, as exemplified by the GLP-1 agonist semaglutide. Fibroblast growth factor 21 (FGF21), a novel metabolic regulator, plays pivotal roles in lipid mobilization and energy conversion, reducing lipotoxicity, inflammation, mitochondrial health, and subsequent tissue damage in organs such as the liver, pancreas, and heart.
View Article and Find Full Text PDFAnn Pharmacother
March 2025
Collegium Medicum, Jan Kochanowski University, Kielce, Poland.
Objective: To summarize the current knowledge on the therapeutic potential of GLP-1 receptor agonists in managing metabolic associated steatotic liver disease (MASLD).
Data Sources: A literature review was conducted using the search terms , , , , , and on PubMed (from January 1, 2019, through February 1, 2025), National Institutes of Health (NIH) (from January 1, 2019, through February 1, 2025), Scopus (from January 1, 2019, through February 1, 2025), and the World Health Organization (WHO) data.
Study Selection And Data Extraction: All relevant clinical trials, review articles, package inserts, and guidelines evaluating clinically relevant evidence regarding the therapeutic potential of GLP-1 agonists in MASLD were considered for inclusion.
Endokrynol Pol
March 2025
Department of Internal, Autoimmune and Metabolic Diseases, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland.
Introduction: Studies show an association between polycystic ovary syndrome (PCOS) and an increased incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) in this patient group. Diagnostic tools that can screen relevant groups of PCOS' patients for liver disease are still being sought.
Material And Methods: Our study included 242 patients with PCOS diagnosed on the basis of the Rotterdam criteria, which we divided according to phenotypes.
Clin Toxicol (Phila)
March 2025
School of Medicine, University of Kansas School of Medicine, Kansas City, KS, USA.
Circulation
March 2025
Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL. (MF., Z.-D.G., M.D., C.L., K.G., S.E.W., E.B.T.).
Background: Despite the high morbidity and mortality of heart failure with preserved ejection fraction (HFpEF), treatment options remain limited. The HFpEF syndrome is associated with a high comorbidity burden, including high prevalence of obesity and hypertension. Although inflammation is implicated to play a key role in HFpEF pathophysiology, underlying causal mechanisms remain unclear.
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