Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut–liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host’s immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut–liver axis in ALD and NAFLD.

Cholangiopathies encompass various biliary diseases affecting the biliary epithelium, resulting in cholestasis, inflammation, fibrosis, and ultimately liver cirrhosis. Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are the most important progressive cholangiopathies in adults. Much research has broadened the scope of disease biology to genetic risk, epigenetic changes, dysregulated mucosal immunity, altered biliary epithelial cell function, and dysbiosis, all of which interact and arise in the context of ill-defined environmental triggers. An in-depth understanding of the molecular pathogenesis of these cholestatic diseases will help clinicians better prevent and treat diseases. In this review, we focus on the main underlying mechanisms of disease initiation and progression, and novel targeted therapeutics beyond currently approved treatments.

obesity is associated with a high risk of morbidity and mortality in the general population and is a major independent risk factor for cardiovascular disease. We sought to evaluate the effect of overweight/ obesity on clinical outcomes of patients with vasospastic angina (VA) at 1-year follow-up. The VA-KOREA (Vasospastic Angina in Korea) registry was a cohort of 11 centers from 2010 to 2015. The primary endpoint was a composite of cardiac death (cD), new-onset arrhythmia, and acute coronary syndrome (ACS). Using the body mass index (BMI) cut-off for Asians, 517 patients with definite VA were divided into either an overweight/obese (BMi ≥ 23 kg/m 2 ) group (n = 378) or a normal weight (BMI 18.5-22.9 kg/m 2 ) group (n = 139). The overweight/obese group showed a significantly lower rate of the primary endpoint composite (2.4% vs 7.9%, p = 0.004) and ACS (0.8% vs 4.3%, p = 0.007) than the normal weight group in the crude population. Similarly, in propensity-score matched analysis, the overweight/obese group showed a significantly lower rate of the primary endpoint composite (2.3% vs 8.4%, p = 0.006) and ACS (1.1% vs 4.6%, p = 0.035) than the normal weight group. However, there were no significant differences in CD and new-onset arrhythmia between the two groups in both the crude and propensity-score matched population. independent predictors of the primary endpoint were overweight/obesity and dyslipidemia. in patients with VA, the overweight/obese group was associated with a favorable 1-year primary endpoint and the difference was mainly driven by the lower rate of ACS compared with the normal weight group.