Decreased plasma endogenous soluble RAGE, and enhanced adipokine secretion, oxidative stress and platelet/coagulative activation identify non-alcoholic fatty liver disease among patients with familial combined hyperlipidemia and/or metabolic syndrome

Santilli, Francesca; Blardi, Patrizia; Scapellato, Carlo; Bocchia, Monica; Guazzi, Gianni; Terzuoli, Lucia; Tabucchi, Antonella; Silvietti, Antonella; Lucani, Benedetta; Gioffrè, Walter Renato; Scarpini, Francesca; Fazio, Francesca; Davı̀, Giovanni; Puccetti, Luca

doi:10.1016/j.vph.2015.04.004

Cited by 29 publications

(18 citation statements)

References 49 publications

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“…According to the evidences already discussed, Yan and coworkers demonstrated a linkage between CAD and HMGB1 serum levels in diabetic and non-diabetic patients, showing that HMGB1 levels was elevated in diabetic and non-diabetic patients with CAD [37]. Furthermore, HMGB1 levels correlated with IL-6, TNF-α and high sensitivity C-reactive protein (hsCRP) and patients with CAD had a decreased level of esRAGE [37], which could correlate with an enhanced inflammatory state [75].…”

Section: Hmgb1 and Diabetic Coronary Artery Diseasementioning

confidence: 96%

High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives

Biscetti

Rando

Nardella

et al. 2019

IJMS

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Diabetes mellitus (DM) is an endemic disease, with growing health and social costs. The complications of diabetes can affect potentially all parts of the human body, from the heart to the kidneys, peripheral and central nervous system, and the vascular bed. Although many mechanisms have been studied, not all players responsible for these complications have been defined yet. High Mobility Group Box-1 (HMGB1) is a non-histone nuclear protein that has been implicated in many pathological processes, from sepsis to ischemia. The purpose of this review is to take stock of all the most recent data available on the role of HMGB1 in the complications of DM.

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Section: Hmgb1 and Diabetic Coronary Artery Diseasementioning

confidence: 96%

High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives

Biscetti

Rando

Nardella

et al. 2019

IJMS

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“…In this edition of Vascular Pharmacology , Santilli and colleagues cross-sectionally compared 60 patients with and 50 patients without non-alcoholic fatty liver disease (NAFLD) [22]. Within these groups were subjects with familial combined hyperlipidemia alone or with metabolic syndrome.…”

Section: Soluble Forms Of Rage: Tracking Receptor Activity In Health mentioning

confidence: 99%

Soluble RAGEs — Prospects for treating & tracking metabolic and inflammatory disease

Schmidt

2015

Vascular Pharmacology

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Emerging evidence links the receptor for advanced glycation endproducts (RAGE) to the pathogenesis of tissue damage in chronic metabolic and inflammatory diseases. In human subjects, multiple reports suggest that in the plasma/serum, circulating levels of distinct forms of soluble RAGEs may be biomarkers of the presence or absence, and the extent of chronic disease. These considerations prompt us to consider in this review, what are soluble RAGEs; how are they formed; what might be their natural functions; and may they serve as biomarkers of inflammatory and metabolic disease activity? In this brief review, we seek to address what is known and suggest new areas for scientific investigation to uncover the biology of soluble RAGEs.

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“…[33] Santilli et al have identified the risk of cardiometabolic disorders to become additive with both metabolic syndrome or FCHL traits only once these patients lost a so-called "protective gene cluster", thus signifying that specific gene abnormalities are more associated with certain traits than simpler concept of monogenic inheritance. [34] The most associated USF1 on chromosome-1 is also linked with both metabolism of lipids and glucose like PPAR-gamma, HNA4a and PTEN, so it's very probable that some of the common symptomatology of FCHL related to USF1 region with metabolic syndrome could be because of this multiple transcription factor regulation and associated signaling mechanisms. [35] Table-3 shows provides an insight into the biochemical alterations in FCHL in comparison to metabolic syndrome.…”

Section: Fchl and Metabolic Syndromementioning

confidence: 99%

Molecular and Metabolic Pathogenesis of Familial Combined Hyperlipidemia and Association with Metabolic Syndrome

Khan

2019

JGM

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Background The objective of this review is to unify the various genetic defects along with elaborating metabolic pathways in Familial Combined Hyperlipidemia(FCHL) and also to differentiate the phenotype of FCHL from metabolic syndrome. Methods PubMed and Cochrane’s library was searched for keyword “Familial combined hyperlipidemia” and latter with “Familial combined hyperlipidemia genes” to finally shortlist 23 articles. Further search with key words “molecular pathogenesis of familial combined hyperlipidemia” and “metabolic syndrome and familial combined hyperlipidemia” was carried out for finding molecular defects in FCHL, non-molecular findings distinguishing FCHL from metabolic syndrome and overlapping features between FCHL and metabolic syndrome. Results Major culprit regions identified included Chromosome-1q21-q24(USF1 and FOXA2) , Ch-11q (APOA5), Ch-16q24, Ch-20q12-q13.1, Ch.4q32.3 (rs6829588), and Ch-19q13.32 containing PVRL-2 gene (Also known as Nectin-2). The genetic and metabolic pathways linked to FCHL may involve: 1-Defective clearance of Apo-B containing lipoproteins, 2-Overproduction of Apo-B containing lipoprotein i.e., VLDL and 3-Adipose tissue dysfunction. FCHL phenotype showed close resemblance with metabolic syndrome clinical and biochemical features with slight differences. Conclusion The reviewed data suggested that FCHL phenotype is the resultant end outcome from multiple molecular defects and thus underlying genetic defect identification in the index case is important for personalized medicine and incoming gene therapy. Further research is warranted to explore specific genetic defects.

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Decreased plasma endogenous soluble RAGE, and enhanced adipokine secretion, oxidative stress and platelet/coagulative activation identify non-alcoholic fatty liver disease among patients with familial combined hyperlipidemia and/or metabolic syndrome

Cited by 29 publications

References 49 publications

High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives

High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives

Soluble RAGEs — Prospects for treating & tracking metabolic and inflammatory disease

Molecular and Metabolic Pathogenesis of Familial Combined Hyperlipidemia and Association with Metabolic Syndrome

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