Heart failure is the terminal outcome of the majority of cardiovascular diseases, which lacks specific diagnostic biomarkers and therapeutic targets. It contributes to most of cardiovascular hospitalizations and death despite of the current therapy. Therefore, it is important to explore potential molecules improving the diagnosis and treatment of heart failure. MicroRNAs (miRNAs) are small non-coding RNAs that have been reported to be involved in regulating processes of heart failure. After the discovery of miRNAs in exosomes, the subcellular distribution analysis of miRNAs is raising researchers' attention. Growing evidence demonstrates that exosomal miRNAs may be promising diagnostic and therapeutic molecules for heart failure. This review summarizes the role of exosomal miRNAs in heart failure in the prospect of molecular and clinical researches.

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Background Recent studies have reported the effects of metabolic syndrome (MetS) and its components on atrial fibrillation (AF), but the results remain controversial. Therefore, we performed a meta-analysis to evaluate the relationship between MetS and AF risk. Methods Studies were searched from the Cochrane library, PubMed, and Embase databases through May 2020. Adjusted hazard ratios (HRs) and its corresponding 95% confidence intervals (CIs) were extracted and then pooled by using a random effects model. Results A total of 6 observational cohort studies were finally included. In the pooled analysis, MetS was associated with an increased risk of AF (HR 1.57; 95% CI 1.40–1.77; P < 0.01). And the components of MetS including abdominal obesity (HR 1.37; 95% CI 1.36–1.38; P < 0.01), elevated blood pressure (HR 1.56; 95% CI 1.46–1.66; P < 0.01), elevated fasting glucose (HR 1.18; 95% CI 1.15–1.21; P < 0.01) and low high density cholesterol (HDL) (HR 1.18; 95% CI 1.06–1.32; P < 0.01) was also associated with an increased risk of AF, while high triglyceride (HR 0.99; 95% CI 0.87–1.11, P = 0.82) was not. Conclusions Our present meta-analysis suggested that MetS, as well as its components including abdominal obesity, elevated blood pressure, elevated fasting glucose and low HDL cholesterol were associated with an increase in the risk of AF.

Aims Coexisting of atrial fibrillation (AF) in patients with heart failure with preserved ejection fraction (HFpEF) could increase the risk of mortality. In this study, we aimed to assess the values of the CHADS2, R2CHADS2, and CHA2DS2-VASc scores for AF prediction in HFpEF patients. Methods and results We performed a retrospective analysis on symptomatic HFpEF patients in the TOPCAT (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist) trial. Associations of the CHADS2, R2CHADS2, and CHA2DS2-VASc scores with the risk of incident AF in HFpEF patients without baseline AF (n = 2202) were assessed using the multivariable competing risk regression models. The discriminatory performances of these scores were calculated using the C-index. During a median follow-up of 3.3 years, the average incidence of AF was 1.80 per 100 patient-years in HFpEF patients. When score was analysed as a continuous variable, per 1-point increase in the CHADS2 (hazard ratio [

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Background Triglyceride-glucose (TyG) index is a reliable surrogate marker of insulin resistance (IR), whereas IR has been implicated in Alzheimer’s disease (AD) pathophysiology. However, the relationship between the TyG index and AD remains unclear. Herein, we aimed to evaluate the associations of both baseline level and long-term trajectories of the TyG index with the risk of AD. Methods This prospective study included 2,170 participants free of AD from the Framingham Heart Study Offspring cohort. The TyG index was calculated as Ln[fasting triglyceride (mg/dL)×fasting glucose (mg/dL)/2]. Data for the TyG index from three examinations were used to identify the long-term trajectories of the TyG index by latent class growth mixture modeling analysis. The Cox and logistic regression models were applied to evaluate the associations of the baseline level and long-term trajectories of the TyG index with AD. Results During a median follow-up of 13.8 years, 163 (7.5%) participants developed AD. Each unit increment of baseline TyG index was associated with a 39% increased risk of AD (adjusted hazard ratio [HR] 1.39, 95% confidence interval [CI] 1.02–1.88). When compared with the reference (TyG index ≤ 8.28), we observed a significantly elevated risk of AD in the group with TyG index of 8.68–9.09 (adjusted HR 1.69, 95% CI 1.03–2.77). In addition, three long-term trajectories of the TyG index were identified (low-stable [95.3%], intermediate-remitting [2.1%], and high-decreasing [2.6%] trajectory group). There was no significant difference in AD risk among the three groups. Conclusions Our findings first showed that a higher baseline TyG index was associated with an increased incidence of AD. The TyG index might be used as a simple surrogate marker for the early detection of AD.

Cardiac hypertrophy is a pathophysiological response to harmful stimuli. The continued presence of cardiac hypertrophy will ultimately develop into heart failure. The mitochondrion is the primary organelle of energy production, and its dysfunction plays a crucial role in the progressive development of heart failure from cardiac hypertrophy. Hispidulin, a natural flavonoid, has been substantiated to improve energy metabolism and inhibit oxidative stress. However, how hispidulin regulates cardiac hypertrophy and its underlying mechanism remains unknown. We found that hispidulin significantly inhibited pressure overload-induced cardiac hypertrophy and improved cardiac function in vivo and blocked phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. We further proved that hispidulin remarkably improved mitochondrial function, manifested by increased electron transport chain (ETC) subunits expression, elevated ATP production, increased oxygen consumption rates (OCR), normalized mitochondrial morphology, and reduced oxidative stress. Furthermore, we discovered that Sirt1, a well-recognized regulator of mitochondrial function, might be a target of hispidulin, as evidenced by its upregulation after hispidulin treatment. Cotreatment with EX527 (a Sirt1-specific inhibitor) and hispidulin nearly completely abolished the antihypertrophic and protective effects of hispidulin on mitochondrial function, providing further evidence that Sirt1 could be the pivotal downstream effector of hispidulin in regulating cardiac hypertrophy.