Aging promotes most degenerative pathologies in mammals, which are characterized by progressive decline of function at molecular, cellular, tissue, and organismal levels and account for a host of health care expenditures in both developing and developed nations. Sarcopenia is a prominent age-related disorder in musculoskeletal system. Defined as gradual and generalized chronic skeletal muscle disorder, sarcopenia involves accelerated loss of muscle mass, strength and function, which is associated with increased adverse functional outcomes and evolutionally refers to muscle wasting accompanied by other geriatric syndromes. More efforts have been made to clarify mechanisms underlying sarcopenia and new findings suggest that it may be feasible to delay age-related sarcopenia by modulating fundamental mechanisms such as cellular senescence. Cellular senescence refers to the essentially irreversible growth arrest mainly regulated by p53/p21^CIP1 and p16^INK4a/pRB pathways as organism ages, possibly detrimentally contributing to sarcopenia via muscle stem cells (MuSCs) dysfunction and the senescence-associated secretory phenotype (SASP) while cellular senescence may have beneficial functions in counteracting cancer progression, tissue regeneration and wound healing. By now diverse studies in mice and humans have established that targeting cellular senescence is a powerful strategy to alleviating sarcopenia. However, the mechanisms through which senescent cells contribute to sarcopenia progression need to be further researched. We review the possible mechanisms involved in muscle stem cells (MuSCs) dysfunction and the SASP resulting from cellular senescence, their associations with sarcopenia, current emerging therapeutic opportunities based on targeting cellular senescence relevant to sarcopenia, and potential paths to developing clinical interventions genetically or pharmacologically.

A number of epidemiological studies have examined the effect of meat consumption on depression. However, no conclusion has been reached. The aim of this study was to examine the relationship between meat consumption and depression. The electronic databases of PUBMED and EMBASE were searched up to March 2017, for observational studies that examined the relationship between meat consumption and depression. The pooled odds ratio (OR) for the prevalence of depression and the relative risk (RR) for the incidence of depression, as well as their corresponding 95% confidence interval (CI), were calculated respectively (the highest versus the lowest category of meat consumption). A total of eight observational studies (three cross-sectional, three cohort and two case-control studies) were included in this meta-analysis. Specifically, six studies were related to the prevalence of depression, and the overall multi-variable adjusted OR suggested no significant association between meat consumption and the prevalence of depression (OR = 0.89, 95% CI: 0.65 to 1.22; P = 0.469). In contrast, for the three studies related to the incidence of depression, the overall multi-variable adjusted RR evidenced an association between meat consumption and a moderately higher incidence of depression (RR = 1.13, 95% CI: 1.03 to 1.24; P = 0.013). Meat consumption may be associated with a moderately higher risk of depression. However, it still warrants further studies to confirm such findings due to the limited number of prospective studies.

Osteoarthritis (OA), one of the most common degenerative diseases, is characterized by progressive degeneration of the articular cartilage and subchondral bone, as well as the synovium. Integrins, comprising a family of heterodimeric transmembrane proteins containing α subunit and β subunit, play essential roles in various physiological functions of cells, such as cell attachment, movement, growth, differentiation, and mechanical signal conduction. Previous studies have shown that integrin dysfunction is involved in OA pathogenesis. This review article focuses on the roles of integrins in OA, especially in OA cartilage, subchondral bone and the synovium. A clear understanding of these roles may influence the future development of treatments for OA.

Background: The associations of whole grain and refined grain consumption with metabolic syndrome (MetS) has been evaluated in several epidemiological studies with conflicting results. This meta-analysis was therefore employed to further investigate the above associations.Method: We searched the PubMed, Web of Science and Embase database until March 2021 (without restriction for inclusion time), for observational studies on the associations of whole grain and refined grain consumption with MetS. The pooled relative risk (RR) of MetS for the highest vs. lowest category of whole grain and refined grain consumption, as well as their corresponding 95% confidence interval (CI) were calculated.Results: A total of 14 observational studies, which involved seven cross-sectional and seven prospective cohort studies, were identified. Specifically, nine studies were related to whole grain consumption, and the overall multi-variable adjusted RR demonstrated that the whole grain consumption was inversely associated with MetS (RR = 0.80, 95%CI: 0.67–0.97; P = 0.021). With regard to refined grain consumption, 13 studies were included. The overall multi-variable adjusted RR indicated that refined grain consumption was positively associated with MetS (RR = 1.37, 95%CI: 1.02–1.84; P = 0.036).Conclusions: The existing evidence suggests that whole grain consumption is negatively associated with MetS, whereas refined grain consumption is positively associated with MetS. Our result might be helpful to better consider the diet effect on MetS. However, more well-designed prospective cohort studies are needed to elaborate the concerned issues further.

Objective: Our aim was to examine the relationship between nut consumption and metabolic syndrome (MetS). Methods: The electronic databases of PubMed, Web of Science, and Embase were searched up to November 2018 for observational studies on the relationship between nut consumption and MetS. The pooled relative risk (RR) of MetS for the highest versus lowest category of nut consumption, as well as their corresponding 95% confidence intervals (CIs) were calculated. Results: A total of 11 observational studies (6 cross-sectional and 5 prospective cohort studies), which involved a total of 89,224 participants, were identified for this meta-analysis. The overall multivariable adjusted RR showed that nut consumption was negatively associated with MetS (RR = 0.84; 95% CI, 0.76-0.92; p < 0.001). Of interest, subgroup analysis confirmed that such findings existed in tree nuts (RR = 0.97; 95% CI, 0.94-1.00; p = 0.04), but not in peanuts (RR = 1.01; 95% CI, 0.96-1.06; p = 0.68). Conclusions: The existing evidence suggested that nut consumption was negatively associated with MetS. However, such an inverse relationship only existed in tree nuts, not in peanuts. More well-designed studies with detailed specifications of nut varieties are needed to further elaborate the issues examined in this study.

Objective: The associations of dietary vitamin C and E intake with depression remains conflicting. This meta-analysis of observational study was therefore employed to clarify the issue further.Methods: An extensive literature review (PubMed, Web of Science and Embase) was performed in January 2022 to identify the observational studies on the associations of dietary vitamin C and E intake with depression. The pooled relative risk (RR) of depression for the highest versus lowest dietary vitamin C and E intake category, and the weighted mean difference (WMD) of dietary vitamin C and E intake for depression versus control subjects, were calculated.Results: A total of 25 observational studies (91966 participants) were included in this meta-analysis. The overall multi-variable adjusted RR demonstrated that dietary vitamin C intake was inversely associated with depression (RR = 0.72, 95% CI: 0.57 to 0.91; P = 0.005). In addition, the combined WMD showed that the dietary vitamin C intake in depression was lower than that in control subjects (WMD = −11.58, 95% CI: −14.88 to −8.29; P < 0.001). Similarly, the overall multi-variable adjusted RR demonstrated that dietary vitamin E intake was negatively associated with depression (RR = 0.84, 95% CI: 0.72 to 0.98; P = 0.02). Moreover, the combined WMD showed that the dietary vitamin E intake in depression was also lower than that in control subjects (WMD = −0.71, 95% CI: −1.07 to −0.34; P < 0.001).Conclusion: The results of this meta-analysis suggest that both dietary vitamin C and E intake is inversely associated with depression. However, due to the limited evidence, more well-designed prospective cohort studies are still needed.