The SARS-CoV-2 virus was first identified at the end of December 2019, causing the disease known as COVID-19, which, due to the high degree of contagion, was declared a global pandemic as of 2020. The end of the isolation was in 2022, thanks to the global multidisciplinary work of the massive vaccination campaigns. Even with the current knowledge about this virus and the COVID-19 disease, there are many questions and challenges regarding diagnosis and therapy in the fight against this virus. One of the big problems is the so-called "long COVID", prolonged symptomatology characterized as a multiorgan disorder manifested as brain fog, fatigue, and shortness of breath, which persist chronically after the disease resolution. Therefore, this review proposes using extracellular vesicles (EVs) as a therapeutic or diagnostic option to confront the sequelae of the disease at the central nervous system level. Development: the review of updated knowledge about SARS-CoV-2 and COVID-19 is generally addressed as well as the current classification of extracellular vesicles and their proposed use in therapy and diagnosis. Through an analysis of examples, extracellular vesicles are highlighted to learn what happens in the central nervous system during and after COVID-19 and as a therapeutic option. Conclusions: even though there are limitations in the knowledge of the neurological manifestations of COVID-19, it is possible to observe the potential use of extracellular vesicles in therapy or as a diagnostic method and even the importance of their study for the knowledge of the pathophysiology of the disease

Metabolic dysfunction–associated steatotic liver disease (MASLD) is defined as the presence of excess triglyceride storage in the liver in the presence of at least one cardiometabolic risk factor. This term highlights the connection between fatty liver and metabolic dysfunction. Dietary factors, such as excessive consumption of saturated fats and sugar, contribute significantly to the accumulation of lipids in organs not specialized for fat storage, such as the liver. Hepatic lipid accumulation initiates dynamic changes in mitochondrial function and promotes the development and progression of MASLD. High‐fat, high‐fructose diet models have provided crucial insights into how nutritional factors induce mitochondrial dysfunction, which is characterized by impaired fatty acid oxidation, excessive generation of reactive oxygen species, and damage to mitochondrial DNA. Lifestyle modifications, including dietary adjustments such as calorie restriction and weight loss, are essential for the early prevention and long‐term treatment of MASLD. However, in recent years, several pharmacological options have emerged for the treatment of MASLD, primarily for the management of its comorbidities. This review explores the mechanisms of mitochondrial dysfunction promoted by the accumulation of hepatic lipids, analyzes the evidence of mitochondrial alterations in the liver of dietary models, and summarizes some of the main therapeutic interventions for MASLD and their effects on mitochondrial function.