Background: Sedentary behavior (SB) and physical activity (PA) are modifiable risk factors for cardiovascular disease (CVD); however, previous research on the effects of PA and SB on CVD has been relatively homogeneous. Our study investigated the association between PA, SB, and CVD-related outcomes.Methods: A comprehensive search strategy was conducted in the MEDLINE, Embase, Cochrane Library, and Web of Science databases from their inception to September 2022. We identified eligible studies according to PICOS: the populations comprised healthy adults, the interventions or exposures were PA or SB, the outcomes were CVD-related outcomes, and the study designs were randomized controlled trials (RCTs) and longitudinal studies (LS). Outcomes were pooled using fixed or random effects models, and the quality of individual studies was assessed by the Cochrane Risk of Bias Instrument and the Newcastle Ottawa Scale.Results: A total of 148 RCTs and 36 LS were included, comprising a total of 75,075 participants. The study quality was rated as low to moderate. We found an increased hazard ratio (HR) for CVD in the population with SB (HR = 1.34; 95% confidence interval [CI]: 1.26 to 1.43; I² = 52.3%; P_{heterogeneity} < 0.001, random model) and a decreased HR for CVD in those who performed long-term PA (HR = 0.71; 95% CI: 0.66 to 0.77; I² = 78.0%, P_{heterogeneity} < 0.001, random model). Long-term PA improved the lipid profiles in healthy adults; participants in this group exhibited increased high-density lipoprotein (weighted mean difference [WMD] = 2.38; 95% CI: 1.00 to 3.76; I² = 84.7%; P_{heterogeneity} < 0.001, random model), decreased triglycerides (WMD = −7.27; 95% CI: −9.68 to −4.87; I² = 0%, P_{heterogeneity} = 0.670, fixed model), and lower total-cholesterol (WMD = −6.84; 95% CI: −9.15 to −4.52; I² = 38.4%, P_{heterogeneity} < 0.001, random model).Conclusions: Long-term SB increases the risk of CVD in healthy adults, whereas PA reduces the risk of CVD and improves indicators associated with CVD. However, the ability of PA to improve blood lipids appeared to be limited. The detailed association of SB and PA on CVD needs to be further investigated in the future.

Exercise has an effect on the reduction of myocardial fibrosis in diabetic rats as previously reported, in which oxidative stress and the TGF-β1/Smad signaling pathway may play key roles. There is little direct experimental evidence that exercise alleviates myocardial fibrosis in type 2 diabetes mellitus (T2DM). Here we established a type 2 diabetic model by using streptozotocin and a high-fat diet. Rats were divided into groups of normal control (NC), T2DM and T2DM plus exercise (T2DME). The T2DME group received further treadmill training at moderate intensity for 8 weeks. Histological and biochemical methods were used to detect the benefits of exercise to T2DM. Results showed that the weight of rats in the T2DM group dropped dramatically, along with significant increases in blood glucose, myocardial fibrosis and oxidative stress, associated with upregulated expression of factors of myocardial fibrosis, except Smad7. Exercise largely reversed T2DM-induced alterations in factors of myocardial fibrosis, including suppressing expression of MMP-2, CTGF, TGF-β1, p-Smad2 and p-Smad3, and increased expression of TIMP–1 and Smad7. Therefore, exercise might be considered an alternative therapeutic remedy for diabetic cardiomyopathy.

Background: To critically evaluate the effects of massage therapy on cancer pain. Methods: Nine Chinese and English databases (PubMed, Cochrane Library, Embase, SCOPUS, Web of Science core, China Biomedical Literature Database, China National Knowledge Infrastructure, Wanfang, and VIP) were systematically searched from the inception of databases to November 2022 for randomized controlled trials. According to Cochrane Collaboration, 2 reviewers independently assessed the risk of bias and extracted data from the included studies. All analyses were performed with Review Manager 5.4. Results: Thirteen randomized controlled trials were included in the meta-analysis, containing 1000 patients (498 in the massage therapy group and 502 in the control group). Massage therapy could significantly relieve cancer pain in patients (standardized mean difference = −1.16, 95% confidence interval [−1.39, −0.93], P < .00001), especially those in the perioperative period and those with hematological malignancies. Foot reflexology and hand acupressure had a moderate effect on cancer pain relief, with hand acupressure being more effective. Massage duration of 10 to 30 minutes and a program length of ≥1 week had a better effect and could significantly relieve pain. The occurrence of adverse events was reported in 4 of the 13 studies, all of which were no adverse events. Conclusions: Massage therapy can be used as a complementary alternative therapy to relieve cancer pain in patients with hematological malignancies, breast cancer, and cancers of the digestive system. It is suggested that chemotherapy patients use foot reflexology, and perioperative period patients use hand acupressure. A massage duration of 10 to 30 minutes and a program length of ≥1 week is recommended to achieve better effects.

Previous studies have shown that early exercise preconditioning (EEP) imparts a protective effect on acute cardiovascular stress. However, how mitophagy participates in exercise preconditioning‐ (EP‐) induced cardioprotection remains unclear. EEP may involve mitochondrial protection, which presumably crosstalks with predominant H₂O₂ oxidative stress. Our EEP protocol involves four periods of 10 min running with 10 min recovery intervals. We added a period of exhaustive running and a pretreatment using phosphoinositide 3‐kinase (PI3K)/autophagy inhibitor wortmannin to test this protective effect. By using transmission electron microscopy (TEM), laser scanning confocal microscopy, and other molecular biotechnology methods, we detected related markers and specifically analyzed the relationship between mitophagic proteins and mitochondrial translocation. We determined that exhaustive exercise associated with various elevated injuries targeted the myocardium, oxidative stress, hypoxia‐ischemia, and mitochondrial ultrastructure. However, exhaustion induced limited mitochondrial protection through a H₂O₂‐independent manner to inhibit voltage‐dependent anion channel isoform 1 (VDAC1) instead of mitophagy. EEP was apparently safe to the heart. In EEP‐induced cardioprotection, EEP provided suppression to exhaustive exercise (EE) injuries by translocating Bnip3 to the mitochondria by recruiting the autophagosome protein LC3 to induce mitophagy, which is potentially triggered by H₂O₂ and influenced by Beclin1‐dependent autophagy. Pretreatment with the wortmannin further attenuated these effects induced by EEP and resulted in the expression of proapoptotic phenotypes such as oxidative injury, elevated Beclin1/Bcl‐2 ratio, cytochrome c leakage, mitochondrial dynamin‐1‐like protein (Drp‐1) expression, and VDAC1 dephosphorylation. These observations suggest that H₂O₂ generation regulates mitochondrial protection in EEP‐induced cardioprotection.

Heart aging is the main susceptible factor to coronary heart disease and significantly increases the risk of heart failure, especially when the aging heart is suffering from ischemia-reperfusion injury. Numerous studies with NAD+ supplementations have suggested its use in anti-aging treatment. However, systematic reviews regarding the overall role of NAD+ in cardiac aging are scarce. The relationship between NAD+ signaling and heart aging has yet to be clarified. This review comprehensively summarizes the current studies on the role of NAD+ signaling in delaying heart aging from the following aspects: the influence of NAD+ supplementations on the aging heart; the relationship and cross-talks between NAD+ signaling and other cardiac aging-related signaling pathways; Importantly, the therapeutic potential of targeting NAD+ in delaying heart aging will be discussed. In brief, NAD+ plays a vital role in delaying heart aging. However, the abnormalities such as altered glucose and lipid metabolism, oxidative stress, and calcium overload could also interfere with NAD+ function in the heart. Therefore, the specific physiopathology of the aging heart should be considered before applying NAD+ supplementations. We believe that this article will help augment our understanding of heart aging mechanisms. In the meantime, it provides invaluable insights into possible therapeutic strategies for preventing age-related heart diseases in clinical settings.