Abstract
Metabolic syndrome (MetS) affects the population worldwide and results from several factors such as genetic background, environment and lifestyle. In recent years, an interplay among autophagy, metabolism, and metabolic disorders has become apparent. Defects in the autophagy machinery are associated with the dysfunction of many tissues/organs regulating metabolism. Metabolic hormones and nutrients regulate, in turn, the autophagy mechanism. Autophagy is a housekeeping stress-induced degradation process that ensures cellular homeostasis. High mobility group box 1 (HMGB1) is a highly conserved nuclear protein with a nuclear and extracellular role that functions as an extracellular signaling molecule under specific conditions. Several studies have shown that HMGB1 is a critical regulator of autophagy. This mini-review focuses on the involvement of HMGB1 protein in the interplay between autophagy and MetS, emphasizing its potential role as a promising biomarker candidate for the early stage of MetS or disease’s therapeutic target.
Highlights
Metabolic syndrome (MetS) increases significantly morbidity and all-cause mortality worldwide (Cornier et al, 2008; Alamdari et al, 2020; Watanabe and Kotani, 2020)
High mobility group box 1 (HMGB1) levels are related to inflammation (Cal et al, 2015), insulin resistance (IR), hyperglycemia (Migazzi et al, 2021), and MetS (Jialal et al, 2014; Chen et al, 2020a)
Firstly described in 1963, only in the 1990s autophagy mechanisms were elucidated with identifying autophagy-related genes (ATG) in yeast (Takeshige et al, 1992; Klionsky, 2007; Mizushima, 2018)
Summary
Metabolic syndrome (MetS) increases significantly morbidity and all-cause mortality worldwide (Cornier et al, 2008; Alamdari et al, 2020; Watanabe and Kotani, 2020). The increasing worldwide prevalence of childhood obesity and diabetes in the young (DeBoer, 2019; Weihe and Weihrauch-Blûher, 2019) has promoted the search for biochemical markers of MetS to identify its prodromal phase or to predict the evolutionary risk. Fatty liver disease and diabetes, the principal components of MetS, show dysregulated hepatic autophagy (Zhang et al, 2018; Allaire et al, 2019). In the AT of obese subjects, monocytes polarize to M1 macrophages and display several cytokines (including TNF-α, IL-6, HMGB1) (Zhang et al, 2017). This molecular shift aggravates the chronic inflammatory state and IR. An increased formation of advanced glycation products (AGE) and their signaling via specific receptors (RAGE), including redox mechanisms, mediate vascular dysfunction and end-organ failure in MetS (Fournet et al, 2018)
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