Abstract
Metabolic syndrome (MetS) is highly associated with a modern lifestyle. The prevalence of MetS has reached epidemic proportion and is still rising. The main cause of MetS and finally type 2 diabetes occurrence is excessive nutrient intake, lack of physical activity, and inflammatory cytokines secretion. These factors lead to redistribution of body fat and oxidative and endoplasmic reticulum (ER) stress occurrence, resulting in insulin resistance, increase adipocyte differentiation, and much elevated levels of proinflammatory cytokines. Cellular therapies, especially mesenchymal stem cell (MSC) transplantation, seem to be promising in the MetS and type 2 diabetes treatments, due to their immunomodulatory effect and multipotent capacity; adipose-derived stem cells (ASCs) play a crucial role in MSC-based cellular therapies. In this review, we focused on etiopathology of MetS, especially on the crosstalk between chronic inflammation, oxidative stress, and ER stress and their effect on MetS-related disease occurrence, as well as future perspectives of cellular therapies. We also provide an overview of therapeutic approaches that target endoplasmic reticulum and oxidative stress.
Highlights
Metabolic syndrome— called insulin resistance syndrome or syndrome X—was described for the first time in 1988 [1]
adipose-derived stem cells (ASCs) have an ability to differentiate into cells of mesoderm, including adipocytes, osteocytes, chondrocytes, and myocytes, that exhibit their potential for cell-based therapies [27, 28]
Both populations of mesenchymal stem cell (MSC), because of their immunomodulatory activity and the potential to differentiate into insulin-producing cells, might become a potential therapy strategy in the course of type 2 diabetes and Metabolic syndrome (MetS) [29,30,31]
Summary
Metabolic syndrome— called insulin resistance syndrome or syndrome X—was described for the first time in 1988 [1]. The conditions that have been described as metabolic risk factors of MetS development involve insulin resistance, hypertension, dyslipidemia (hypertriglyceridemia, low high-density lipoprotein cholesterol), abdominal obesity, elevated glucose levels, high blood pressure, and proinflammatory and prothrombotic state [2]. MetS is associated with a high risk of developing several lifestyle diseases including type 2 diabetes and cerebrovascular disease. 8.3% of adults (382 mln) live with type 2 diabetes but the number is still rising. It is estimated that the number of diabetes patients will increase to 592 mln in. We demonstrated the effect of chronic inflammation, oxidative stress, and prolonged endoplasmic reticulum stress on MetS development, as well as the potential of cellular therapy on MetSassociated diseases, especially type 2 diabetes treatment
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