Non-alcoholic fatty liver (NAFLD) is the most common liver disease worldwide, progressing from simple steatosis to necroinflammation and fibrosis (leading to non-alcoholic steatohepatitis, NASH), and in some cases to cirrhosis and hepatocellular carcinoma Inflammation, oxidative stress and insulin resistance are involved in NAFLD development and progression NAFLD has been associated with several cardiovascular (CV) risk factors including obesity, dyslipidemia, hyperglycemia, hypertension and smoking NAFLD is also characterized by atherogenic dyslipidemia, postprandial lipemia and high-density lipoprotein (HDL) dysfunction Most importantly, NAFLD patients have an increased risk for both liver and CV disease (CVD) morbidity and mortality In this narrative review, the associations between NAFLD, dyslipidemia and vascular disease in NAFLD patients are discussed NAFLD treatment is also reviewed with a focus on lipid-lowering drugs Finally, future perspectives in terms of both NAFLD diagnostic biomarkers and therapeutic targets are considered

Non-alcoholic fatty liver disease and dyslipidemia: An update

Liver disease, involving a wide range of liver pathologies from fatty liver, hepatitis, and fibrosis to cirrhosis and hepatocellular carcinoma, is a serious health problem worldwide. In recent years, many natural foods and herbs with abundant phytochemicals have been proposed as health supplementation for patients with hepatic disorders. As an important category of phytochemicals, natural polyphenols have attracted increasing attention as potential agents for the prevention and treatment of liver diseases. The striking capacities in remitting oxidative stress, lipid metabolism, insulin resistance, and inflammation put polyphenols in the spotlight for the therapies of liver diseases. It has been reported that many polyphenols from a wide range of foods and herbs exert therapeutic effects on liver injuries via complicated mechanisms. Therefore, it is necessary to have a systematical review to sort out current researches to help better understand the potentials of polyphenols in liver diseases. In this review, we aim to summarize and update the existing evidence of natural polyphenols in the treatment of various liver diseases by in vitro, in vivo, and clinical studies, while special attention is paid to the action mechanisms.

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The Potential and Action Mechanism of Polyphenols in the Treatment of Liver Diseases.

A wide range of external stress stimuli trigger plant cells to undergo complex network of reactions that ultimately lead to the synthesis and accumulation of secondary metabolites. Accumulation of such metabolites often occurs in plants subjected to stresses including various elicitors or signal molecules. Throughout evolution, endophytic fungi, an important constituent in the environment of medicinal plants, have known to form long-term stable and mutually beneficial symbiosis with medicinal plants. The endophytic fungal elicitor can rapidly and specifically induce the expression of specific genes in medicinal plants which can result in the activation of a series of specific secondary metabolic pathways resulting in the significant accumulation of active ingredients. Here we summarize the progress made on the mechanisms of fungal elicitor including elicitor signal recognition, signal transduction, gene expression and activation of the key enzymes and its application. This review provides guidance on studies which may be conducted to promote the efficient synthesis and accumulation of active ingredients by the endogenous fungal elicitor in medicinal plant cells, and provides new ideas and methods of studying the regulation of secondary metabolism in medicinal plants.

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The regulatory mechanism of fungal elicitor-induced secondary metabolite biosynthesis in medical plants.

Background & Aim
MicroRNAs (miRs) regulate hepatic steatosis, inflammation and fibrosis. Fibrosis is the consequence of chronic tissue damage and inflammation. We hypothesized that deficiency of miR-155, a master regulator of inflammation, attenuates steatohepatitis and fibrosis.

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MicroRNA-155 Deficiency Attenuates Liver Steatosis and Fibrosis without Reducing Inflammation in a Mouse Model of Steatohepatitis

Inflammation is an adaptive response in pursuit of homeostasis reestablishment triggered by harmful conditions or stimuli, such as an infection or tissue damage. Liver diseases cause approximately 2 million deaths per year worldwide and hepatic inflammation is a common factor to all of them, being the main driver of hepatic tissue damage and causing progression from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH), cirrhosis and, ultimately, hepatocellular carcinoma (HCC). The metabolic sensor SIRT1, a class III histone deacetylase with strong expression in metabolic tissues such as the liver, and transcription factor NF-κB, a master regulator of inflammatory response, show an antagonistic relationship in controlling inflammation. For this reason, SIRT1 targeting is emerging as a potential strategy to improve different metabolic and/or inflammatory pathologies. In this review, we explore diverse upstream regulators and some natural/synthetic activators of SIRT1 as possible therapeutic treatment for liver diseases.

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Relevance of SIRT1-NF-κB Axis as Therapeutic Target to Ameliorate Inflammation in Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is a common liver disease, and the incidence increases year by year. The pathogenesis of NAFLD is correlated with insulin resistant (IR), and oxidative stress which induces varied inflammatory cytokines (TNF-α, IL-1, IL-6, etc). Different signal transductions such as MAPK, NF-κB, AMPK, JAK2/STAT3, PPAR, PI3K/Akt, TLR were activated by the pathogenic factors to regulate correlative reactions. Thus, in-depth study of the signal transductions will probably provide new suitable solutions for the prevention and therapy of NAFLD.

Signal transductions and nonalcoholic fatty liver: a mini-review.

Mitochondrial pyruvate carrier 1 regulates fatty acid synthase lactylation and mediates treatment of nonalcoholic fatty liver disease.

Idiopathic pulmonary fibrosis is a diffuse interstitial lung disease of a kind of type, more common in idiopathic interstitial pneumonia, early pathological characteristics are mainly characterized by diffuse alveolar inflammation, alveolar structure disorder late is characterized by abnormal hyperplasia of fibroblasts and extracellular matrix accumulation and collagen content increases, eventually, lead to pulmonary fibrosis (1). The main clinical manifestations of this disease are respiratory disturbance accompanied by irritant dry cough, and there is usually a burst sound at the end of inspiration in the middle and lower part of both lungs (2, 3). Due to the insidious onset of this disease, patients with symptoms usually have a disease history of 1-3 years, and most of them have the symptoms of decreased lung function (4). In recent years, due to increasing air pollution and changes in life and population structure, the incidence of the disease has been increasing year by year all over the world. Strongman et al. (5) made statistics on the morbidity and mortality of patients in the UK, and the results showed that 4527 cases of idiopathic fibrosis were found in 9748108 primary care patients, and the incidence increased by nearly 80% compared with The mechanism of lung tissue YKL-40 promoting the interstitial transformation of alveolar epithelial cells and its effect on TGF-β1 level in mice with idiopathic pulmonary fibrosis

The mechanism of lung tissue YKL-40 promoting the interstitial transformation of alveolar epithelial cells and its effect on TGF-β1 level in mice with idiopathic pulmonary fibrosis

Jin J Yin

Papers

Signal transductions and nonalcoholic fatty liver: a mini-review.

Mitochondrial pyruvate carrier 1 regulates fatty acid synthase lactylation and mediates treatment of nonalcoholic fatty liver disease.

The mechanism of lung tissue YKL-40 promoting the interstitial transformation of alveolar epithelial cells and its effect on TGF-β1 level in mice with idiopathic pulmonary fibrosis