Background: Short or long sleep duration is proposed as a potential risk factor for all-cause mortality in the older people, yet the results of published studies are not often reproducible. Methods: Literature retrieval, study selection and data extraction were completed independently and in duplicate. Only prospective cohort studies were included. Effect-size estimates are expressed as hazard ratio (HR) and 95% confidence interval (CI). Results: Summary data from 28 articles, involving a total of 95,259 older people, were meta-analyzed. Overall analyses revealed a remarkably significant association between long sleep duration and all-cause mortality (adjusted HR = 1.24, 95% CI: 1.16-1.33, P < .001), whereas only marginal significance was observed for short sleep duration (adjusted HR = 1.04; 95% CI: 1.00-1.09; P = .033). Funnel plots suggested no publication bias for short sleep duration (P = .392). The probability of publication bias was high for long sleep duration (P = .020), yet the trim-and-fill method strengthened its significance in predicting all-cause mortality. In subgroup analyses, the association of long sleep duration with all-cause mortality was statistically significant in both women (HR = 1.48; 95% CI: 1.18-1.86; P = .001) and men (HR = 1.31; 95% CI: 1.10-1.58; P = .003). By contrast, with regard to short sleep duration, statistical significance was observed in men (HR = 1.13; 95% CI: 1.04-1.24; P = .007), but not in women (HR = 1.00; 95% CI: 0.85-1.18; P = .999) (Two-sample Z test P = .099). Besides gender, geographic region, sleep survey method, baseline age and follow-up interval were identified as possible causes of between-study heterogeneity in subgroup analyses. Further dose-response regression analyses revealed that trend estimation was more obvious for long sleep duration (regression coefficient: 0.13; P < .001) than for short sleep duration (regression coefficient: 0.02; P = .046). Conclusions: Our findings indicate a significantly increased risk of all-cause mortality associated with long sleep duration, especially in women, as well as with short sleep duration in men only.

Aims. The aim of this meta-analysis was to comprehensively evaluate the association of early age at natural menopause with the risk for all-cause and cardiovascular mortality. Methods. Literature retrieval was done on August 4, 2020. Article selection and data extraction were completed independently and in duplicate. Early age at natural menopause was grouped into premature menopause (<40 years), early menopause (40-44 years), and relatively early menopause (45-49 years). Effect-size estimates are summarized as hazard ratio (HR) or relative risk (RR) with 95% confidence interval (CI). Results. Sixteen articles involving 321,233 women were meta-analyzed. Overall analyses revealed a statistically significant association of early age at natural menopause with all-cause mortality risk ( H R adjusted = 1.08 , 95% CI: 1.03 to 1.14, P = 0.002 ; R R adjusted = 1.05 , 95% CI 1.01 to 1.08, P = 0.005 ), but not with cardiovascular mortality risk. In dose-response analyses, the association with all-cause mortality was significant for premature menopause with ( H R adjusted = 1.10 ; 95% CI: 1.01 to 1.21; P = 0.034 ) and without ( R R adjusted = 1.34 ; 95% CI: 1.08 to 1.66; P = 0.007 ) considering follow-up intervals. As for cardiovascular mortality, marginal significance was noted for premature menopause after considering follow-up intervals ( HR = 1.09 ; 95% CI: 1.00-1.19; P = 0.045 ). Subgroup analyses indicated that gender, country, and follow-up periods were possible causes of heterogeneity. There was an overall low probability of publication bias. Conclusions. Our findings indicate that premature menopause is a promising independent risk factor for both all-cause and cardiovascular mortality.

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Mitophagy is a type of autophagy that can selectively eliminate damaged and depolarized mitochondria to maintain mitochondrial activity and cellular homeostasis. Several pathways have been found to participate in different steps of mitophagy. Mitophagy plays a significant role in the homeostasis and physiological function of vascular endothelial cells, vascular smooth muscle cells, and macrophages, and is involved in the development of atherosclerosis (AS). At present, many medications and natural chemicals have been shown to alter mitophagy and slow the progression of AS. This review serves as an introduction to the field of mitophagy for researchers interested in targeting this pathway as part of a potential AS management strategy.