Background: Studies have demonstrated that remnant cholesterol is correlated with the risk of ischemic stroke. However, it is unknown whether visit-to-visit variability in remnant cholesterol concentration affects ischemic stroke. We sought to examine the role of remnant cholesterol variability in the subsequent development of ischemic stroke in the general population. Methods: We performed a post hoc analysis including eligible participants from the Kailuan Study cohort who underwent 3 health examinations and were free of atrial fibrillation, myocardial infarction, stroke, cancer, or known lipid-medication use from 2006 to 2010. Participants were followed up until the end of 2017. Variability was quantified as variability independent of the mean, average real variability, and SD. Multivariate analysis was performed using the Fine and Gray competing risk model to estimate subhazard ratios assuming death as a competing risk. Results: The final study cohort comprised 38 556 participants. After a median follow-up of 7.0 years, 1058 individuals were newly diagnosed with ischemic stroke. After adjusting for age (time scale), sex, smoking status, alcohol consumption, physical activity, hypertension, diabetes, family history of cardiovascular disease, body mass index, estimated glomerular filtration rate, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and mean remnant cholesterol, the highest quartile (quartile 4) of variability independent of the mean of remnant cholesterol was associated with an increased ischemic stroke risk compared with the lowest quartile (quartile 1), (subhazard ratio, 1.27 [95% CI, 1.06–1.53]). For each 1-SD increase in variability independent of the mean of remnant cholesterol, the risk increased by 9% (subhazard ratio, 1.09 [95% CI, 1.03–1.16]). The association was also significant using average real variability and SD as indices of variability. Conclusions: Greater remnant cholesterol variability was associated with a higher risk of ischemic stroke in the general population.

Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decay in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the aging process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death pathway characterized by excessive iron accumulation followed by the generation of reactive oxygen species (ROS). Oxidative stress is a common trigger of this condition and may be induced by various factors such as toxins, drugs, and inflammation. Ferroptosis is linked to numerous disorders, including cardiovascular disease, neurodegeneration, and cancer. Senescence is believed to contribute to the decay in tissue and organ functions occurring with aging. It has also been linked to the development of age-related pathologies, such as cardiovascular diseases, diabetes, and cancer. In particular, senescent cells have been shown to produce inflammatory cytokines and other pro-inflammatory molecules that can contribute to these conditions. In turn, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer. Ferroptosis is known to play a role in the development of these pathologies by promoting the death of damaged or diseased cells and contributing to the inflammation often associated. Both senescence and ferroptosis are complex pathways that are still not fully understood. Further research is needed to thoroughly investigate the role of these processes in aging and disease, and to identify potential interventions to target such processes in order to prevent or treat age-related conditions. This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, aging, and disease, and whether they can be exploited to block or limit the decay of the physiological functions in elderly people for a healthy longevity.

Aims/Introduction: A higher ratio of triglyceride to high‐density lipoprotein cholesterol (TG/HDL‐C) is considered as the independent risk index of cardiovascular (CV) events. However, cohort studies regarding this correlation are rarely reported, especially in the Chinese population. The aim of present study was to explore the relationship of the TG/HDL‐C ratio with CV risks among Chinese adults during 10‐year follow‐up period.Materials and Methods: We carried out a prospective study using data obtained from 96,542 individuals in Kailuan, who were grouped through the median value (0.8533) of the TG/HDL‐C ratio. Adverse outcomes mainly referred to major CV events. We used the person‐years incidence and cumulative incidence to predict the morbidity. The risk of CV events was estimated through Cox proportional hazard models.Results: The mean age of the cohort was 51.5 ± 12.6 years, and 79.6% of participants were men. During a median follow‐up period of 9.75 years, 5,422 major CV events occurred, including 1,312 myocardial infarction cases and 4,228 stroke cases. The cumulative incidence of myocardial infarction, stroke and total CV events was 1.36% (range 1.29–1.43%), 4.38% (range 4.25–4.51%) and 5.62% (range 5.47–5.76%), respectively. Compared with low the TG/HDL‐C ratio (≤0.8533) group, the high TG/HDL‐C ratio (>0.8533) group had higher morbidity of CV events. The hazard ratio of total CV events, stroke and myocardial infarction was 1.19 (95% CI 1.12–1.26), 1.11 (95% CI 1.03–1.18) and 1.50 (95% CI 1.33–1.70), respectively. Furthermore, the TG/HDL‐C ratio and major CV events had a line‐shaped relationship with each other.Conclusions: Among the Chinese population, a higher TG/HDL‐C ratio is correlated with an increased risk of major CV events.

Background: Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased cellular damage and death. These conditions play an essential role in aging and significantly contribute to the development of age-related complications. Humanin is a mitochondrial-derived peptide (MDP), encoded by mitochondrial DNA, playing a cytoprotective role to preserve mitochondrial function and cell viability under stressful and senescence conditions. For these reasons, humanin can be exploited in strategies aiming to counteract several processes involved in aging, including cardiovascular disease, neurodegeneration, and cancer. Relevance of these conditions to aging and disease: Senescence appears to be involved in the decay in organ and tissue function, it has also been related to the development of age-related diseases, such as cardiovascular conditions, cancer, and diabetes. In particular, senescent cells produce inflammatory cytokines and other pro-inflammatory molecules that can participate to the development of such diseases. Humanin, on the other hand, seems to contrast the development of such conditions, and it is also known to play a role in these diseases by promoting the death of damaged or malfunctioning cells and contributing to the inflammation often associated with them. Both senescence and humanin-related mechanisms are complex processes that have not been fully clarified yet. Further research is needed to thoroughly understand the role of such processes in aging and disease and identify potential interventions to target them in order to prevent or treat age-related conditions. Objectives: This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, humanin, aging, and disease.

On the basis of 45,092 participants (mean age of 54.04 ± 13.09 years) from the Kailuan study, this study was performed to explore the relationships among total cholesterol (TC), brachial-ankle pulse wave velocity (BaPWV), and systolic blood pressure (SBP) and quantify their separate effects. The correlations among TC, SBP, and BaPWV were analyzed using multivariate linear regression models. Mediation analysis was performed to determine whether the effect of TC on SBP can be explained by arterial stiffness. Multivariate linear regression analysis showed that for every one standard deviation increase in TC and BaPWV, SBP increased by 0.33 mmHg and 0.044 mmHg, respectively; for every one standard deviation increase in TC, BaPWV increased by 5.34 cm/s. Mediation analysis showed that the TC-induced SBP elevation was mediated by arterial stiffness in more than half of the whole cohort (indirect effect, 0.73; percent mediated, 54.5%). Furthermore, the TC-induced SBP elevation was mediated by arterial stiffness in less than half of the males (indirect effect, 0.70; percent mediated, 47.9%); however, the results were not statistically significant in females. In conclusion, TC and BaPWV are positively correlated with SBP, whereas TC is positively correlated with BaPWV. Almost half of the increase in SBP contributed to TC is mediated by arterial stiffness.

Objective The aim of this study was to examine the association between age at onset of overweight and incident hypertension. Methods We analysed 4742 participants with new-onset overweight from the Kailuan study between 2006 and 2015 and and 4742 age-matched and sex-matched controls selected randomly from the same cohort but with normal weight. Participants were compared with respect to subsequent risk of hypertension, with sub-HR calculated with the Fine and Gray model, according to age of onset of overweight. Results Over a mean follow-up period of 5.17 years, 1642 overweight participants (34.6%) and 1293 normal-weight controls (27.3%) were subsequently diagnosed with hypertension. The median age at onset of overweight was 49.1 years. Compared with normal-weight controls, the multivariable-adjusted sub-HR for hypertension among participants with onset of overweight at 18–39 years of age, 40–49 years of age, 50–59 years of age and ≥60 years of age was 1.38 (95% CI 1.11 to 1.72), 1.27 (95% CI 1.09 to 1.49), 1.23 (95% CI 1.09 to 1.38) and 1.14 (95% CI 0.99 to 1.32), respectively. Onset of overweight in each age range was significantly associated with increased risk of hypertension, except for the group with onset at ≥60 years of age. The risk increased with each decade of attenuation of age at onset, peaking at 18–39 years of age. Conclusions Younger age at onset of overweight across adulthood was associated with significantly increased risk of hypertension, with the highest relative risk among participants with onset of overweight at 18–39 years of age.