Multiple organs involved in the pathogenesis of non-alcoholic fatty liver disease
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ell & Bioscience Open Access
REVIEW
Multiple organs involved in the pathogenesis of non‑alcoholic fatty liver disease Xiaoyan Li1 and Hua Wang1,2*
Abstract Non-alcoholic fatty liver disease (NAFLD) represents the leading cause of chronic liver disease worldwide and the anticipated health burden is huge. There are limited therapeutic approaches for NAFLD now. It’s imperative to get a better understanding of the disease pathogenesis if new treatments are to be discovered. As the hepatic manifestation of metabolic syndrome, this disease involves complex interactions between different organs and regulatory pathways. It’s increasingly clear that brain, gut and adipose tissue all contribute to NAFLD pathogenesis and development, in view of their roles in energy homeostasis. In the present review, we try to summarize currently available data regarding NAFLD pathogenesis and to lay a particular emphasis on the inter-organ crosstalk evidence. Keywords: Non-alcoholic fatty liver disease, Energy metabolism, Lipid, Hormone, Inter-organ crosstalk Introduction Non-alcoholic fatty liver disease (NAFLD), has been commonly considered as the leading cause of chronic liver diseases in Western countries over the last decade [1]. In the meantime, urbanization in many developing countries has recently led to a sedentary lifestyle and overnutrition, which contribute to obesity, metabolic syndrome and the emerging condition of NAFLD [2]. NAFLD currently has a reported prevalence of 12–38% worldwide and the number is growing inexorably and steadily along with the unprecedented levels of obesity in human society [3]. On account of the radical cure of hepatitis C, the imminent disappearance of hepatitis B and the uncontrolled energy-dense lifestyle, NAFLD would undoubtedly become the mainspring for liver related morbidity and mortality very soon. As estimated, NAFLD should be the most frequent indication for liver transplantation by 2030 [4]. To date, no drug for NAFLD *Correspondence: [email protected] 1 Department of Oncology, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China Full list of author information is available at the end of the article
has received FDA approval, giving rise to insufficient pharmacotherapeutic interventions in clinical practice [5]. These alarming situations necessitate the extension of our understanding towards pathogenic mechanisms of NAFLD. NAFLD could be simply interpreted as the condition where excess fat is stored in the liver, and this secondary fat accumulation is not the consequence of other factors like heavy alcohol consumption, drug side effects or genetic variations [6]. Whether liver inflammation exists is the basis to subdivide NAFLD into two types, fatty liver and non-alcoholic steatohepatitis (NASH), and the latter is the progressive phenotype of NAFLD spectrum [7]. Persistent inflammation will jeopardize liver homeostasis and activate the repair processes. Activated hepatic stellate cells (HSCs) secrete extracellular matrix (ECM), including type 1 collagen, to
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