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  • 1
    Online Resource
    Online Resource
    MDPI AG ; 2022
    In:  International Journal of Molecular Sciences Vol. 23, No. 24 ( 2022-12-16), p. 16053-
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 23, No. 24 ( 2022-12-16), p. 16053-
    Abstract: High mortality rates due to cardiovascular diseases (CVDs) have attracted worldwide attention. It has been reported that mitochondrial dysfunction is one of the most important mechanisms affecting the pathogenesis of CVDs. Mitochondrial DNA (mtDNA) mutations may result in impaired oxidative phosphorylation (OXPHOS), abnormal respiratory chains, and ATP production. In dysfunctional mitochondria, the electron transport chain (ETC) is uncoupled and the energy supply is reduced, while reactive oxygen species (ROS) production is increased. Here, we discussed and analyzed the relationship between mtDNA mutations, impaired mitophagy, decreased OXPHOS, elevated ROS, and CVDs from the perspective of mitochondrial dysfunction. Furthermore, we explored current potential therapeutic strategies for CVDs by eliminating mtDNA mutations (e.g., mtDNA editing and mitochondrial replacement), enhancing mitophagy, improving OXPHOS capacity (e.g., supplement with NAD+, nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), and nano-drug delivery), and reducing ROS (e.g., supplement with Coenzyme Q10 and other antioxidants), and dissected their respective advantages and limitations. In fact, some therapeutic strategies are still a long way from achieving safe and effective clinical treatment. Although establishing effective and safe therapeutic strategies for CVDs remains challenging, starting from a mitochondrial perspective holds bright prospects.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 2
    In: Antioxidants, MDPI AG, Vol. 12, No. 1 ( 2022-12-28), p. 62-
    Abstract: Antioxidant minerals including zinc, copper and selenium play critical roles in the maintenance of the redox balance in the body. However, their influences on type 2 diabetes mellitus (T2DM) are still inconclusive in Chinese populations. To elucidate the relationship between antioxidant minerals and T2DM, serum zinc, copper and selenium concentrations were measured in 1443 Chinese urban residents using a 1:2 matched case-control study. Conditional logistic regression models (CLR) were used to obtain the odds ratios (ORs) and 95% confidence intervals (CIs), and restricted cubic splines (RCS) were used to examine their dose–response associations. Serum zinc (OR = 0.52 [0.35, 0.77]) and copper concentrations (OR = 0.25 [0.17, 0.37] ) were negatively associated with T2DM in a fully adjusted model. An L-shaped zinc-T2DM association (Poverall association = 0.003, and Pnonlinearity = 0.005) and a negative linear copper-T2DM association (Poverall association 〈 0.0001, and Pnonlinearity = 0.395) were observed. No association was found between serum selenium and T2DM in fully adjusted CLR or RCS models. In addition, joint associations with T2DM were identified between serum zinc and copper and between serum selenium and copper. In conclusion, our study emphasizes the importance of an adequate intake of antioxidant minerals for T2DM prevention in the Chinese population.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-7-30)
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-7-30)
    Abstract: Almost three decades after its seminal discovery, our understanding of the remarkable TOR pathway continues to expand. As a TOR complex, TORC2 lies at the nexus of many signaling pathways and directs a diverse array of fundamental processes such as cell survival, proliferation, and metabolism by integrating environmental and intracellular cues. The dysregulation of TORC2 activity disrupts cellular homeostasis and leads to many pathophysiological conditions. With continued efforts at mapping the signaling landscape, the pace of discovery in TORC2 regulation has been accelerated in recent years. Consequently, emerging evidence has expanded the repertoire of upstream regulators and has revealed unexpected diversity in the modes of TORC2 regulation. Multiple environmental cues and plasma membrane proteins that fine-tune TORC2 activity are unfolding. Furthermore, TORC2 signaling is intricately intertwined with other major signaling pathways. Therefore, feedback and crosstalk regulation also extensively modulate TORC2. In this context, we provide a comprehensive overview of revolutionary concepts regarding emerging regulators of TORC2 and discuss evidence of feedback and crosstalk regulation that shed new light on TORC2 biology.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 4
    In: International Journal of Surgery, Ovid Technologies (Wolters Kluwer Health)
    Abstract: Coronary artery bypass grafting (CABG) remains the gold standard for the treatment of multivessel and left main coronary heart disease. However, the current evidence about the optimal surgical revascularization strategy is inconsistent and is not sufficient to allow for definite conclusions. Thus, this topic needs to be extensively discussed. Objective: The aim of this present study was to compare the clinical outcomes of off-pump CABG (OPCAB), conventional on-pump CABG (C-CABG) and on-pump beating heart (ONBEAT) CABG via an updated systematic review and network meta-analysis of randomized controlled trials (RCTs). Data Sources: PubMed, Web of Science and the Cochrane Central Registry were searched for relevant RCTs that were published in English before December 1, 2021. Study Selection Published trials that included patients who received OPCAB, C-CABG and ONBEAT CABG were selected. Data Extraction and Synthesis: Two authors independently screened the search results, assessed the full texts to identify eligible studies and the risk of bias of the included studies, and extracted data. All processes followed the Preferred Reporting Items for Systematic Review and Meta-analysis of Individual Participant Data. Main Outcomes and Measures: The primary outcome was postoperative mortality in patients who underwent C-CABG, OPCAB or ONBEAT CABG. The secondary outcomes were postoperative myocardial infarction, stroke, and renal impairment in the three groups. The time point for analysis of outcomes was all time periods during the postoperative follow-up. Results: A total of 39385 patients (83,496.2 person-years) in 65 studies who fulfilled the prespecified criteria were included. In the network meta-analysis, OPCAB was associated with an increase of 12% in the risk of all-cause mortality when compared with C-CABG (OR: 1.12; 95% CI: 1.04 to 1.21), a reduction of 49% in the risk of myocardial infarction when compared with ONBEAT (OR: 0.51; 95% CI: 0.26 to 0.99), a reduction of 16% in the risk of stroke when compared with C-CABG (OR: 0.84; 95% CI: 0.72 to 0.99) and a similar risk of renal impairment when compared with C-CABG and ONBEAT. Conclusions and Relevance: OPCAB was associated with higher all-cause mortality but lower postoperative stroke compared with C-CABG. OPCAB was associated with lower postoperative myocardial infarction than that of ONBEAT. Early mortality was comparable among OPCAB, ONBEAT and C-CABG.
    Type of Medium: Online Resource
    ISSN: 1743-9159
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2201966-2
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  • 5
    Online Resource
    Online Resource
    Elsevier BV ; 2022
    In:  Journal of the American College of Cardiology Vol. 80, No. 24 ( 2022-12), p. 2269-2285
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 80, No. 24 ( 2022-12), p. 2269-2285
    Type of Medium: Online Resource
    ISSN: 0735-1097
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1468327-1
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  • 6
    In: Nutrients, MDPI AG, Vol. 14, No. 19 ( 2022-10-09), p. 4207-
    Abstract: Casein hydrolysate has various biological functional activities, especially prominent are angiotensin I-converting enzyme inhibitory activities. Increasing evidence has reported the prominent hypotensive effect of casein hydrolysate. However, the effects of casein hydrolysate on cardiovascular risk factors remain unclear and require more comprehensive and detailed studies. Here, we conducted a systematic review and meta-analysis on eligible randomized controlled trials (RCTs) to summarize the effects of casein hydrolysate supplementation on blood pressure, blood lipids, and blood glucose. In the pooled analyses, casein hydrolysate significantly reduced systolic blood pressure by 3.20 mmHg (−4.53 to −1.87 mmHg) and diastolic blood pressure by 1.50 mmHg (−2.31 to −0.69 mmHg). Supplementation of casein hydrolysate displayed no effect on total cholesterol (−0.07 mmol/L; −0.17 to 0.03 mmol/L), low-density lipoprotein cholesterol (−0.04 mmol/L; −0.15 to 0.08 mmol/L), high-density lipoprotein cholesterol (−0.01 mmol/L; −0.06 to 0.03 mmol/L), triglycerides (−0.05 mmol/L, −0.14 to 0.05 mmol/L), or fasting blood glucose (−0.01 mmol/L; −0.10 to 0.09 mmol/L) compared with the placebo diets. Collectively, this study indicated that supplementation of casein hydrolysate displayed decreasing effect on blood pressure without affecting blood lipids or glycemic status.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2518386-2
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  • 7
    Online Resource
    Online Resource
    MDPI AG ; 2022
    In:  Nutrients Vol. 14, No. 24 ( 2022-12-15), p. 5330-
    In: Nutrients, MDPI AG, Vol. 14, No. 24 ( 2022-12-15), p. 5330-
    Abstract: The elderly proportion of the population is gradually increasing, which poses a great burden to society, the economy, and the medical field. Aging is a physiological process involving multiple organs and numerous reactions, and therefore it is not easily explained or defined. At present, a growing number of studies are focused on the mechanisms of aging and potential strategies to delay aging. Some clinical drugs have been demonstrated to have anti-aging effects; however, many still have deficits with respect to safety and long-term use. Polysaccharides are natural and efficient biological macromolecules that act as antioxidants, anti-inflammatories, and immune regulators. Not surprisingly, these molecules have recently gained attention for their potential use in anti-aging therapies. In fact, multiple polysaccharides have been found to have excellent anti-aging effects in different animal models including Caenorhabditis elegans, Drosophila melanogaster, and mice. The anti-aging qualities of polysaccharides have been linked to several mechanisms, such as improved antioxidant capacity, regulation of age-related gene expression, and improved immune function. Here, we summarize the current findings from research related to anti-aging polysaccharides based on various models, with a focus on the main anti-aging mechanisms of oxidative damage, age-related genes and pathways, immune modulation, and telomere attrition. This review aims to provide a reference for further research on anti-aging polysaccharides.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2518386-2
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  • 8
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 14, No. 8 ( 2023-08-08)
    Abstract: Cervical cancer is one of the leading causes of cancer death in women. Mitochondrial-mediated ferroptosis (MMF) is a recently discovered form of cancer cell death. However, the role and the underlying mechanism of MMF in cervical cancer remain elusive. Here, using an unbiased screening for mitochondrial transmembrane candidates, we identified mitochondrial carrier 1 ( MTCH1 ) as a central mediator of MMF in cervical cancers. MTCH1 -deficiency disrupted mitochondrial oxidative phosphorylation while elevated mitochondrial reactive oxygen species (ROS) by decreasing NAD + levels. This mitochondrial autonomous event initiated a mitochondria-to-nucleus retrograde signaling involving reduced FoxO1 nuclear translocation and subsequently downregulation of the transcription and activity of a key anti-ferroptosis enzyme glutathione peroxidase 4 (GPX4), thereby elevating ROS and ultimately triggering ferroptosis. Strikingly, targeting MTCH1 in combination with Sorafenib effectively and synergistically inhibited the growth of cervical cancer in a nude mouse xenograft model by actively inducing ferroptosis. In conclusion, these findings enriched our understanding of the mechanisms of MMF in which MTCH1 governed ferroptosis though retrograde signaling to FoxO1-GPX4 axis, and provided a potential therapeutic target for treating cervical cancer.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2541626-1
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  • 9
    Online Resource
    Online Resource
    MDPI AG ; 2023
    In:  Nutrients Vol. 15, No. 7 ( 2023-03-28), p. 1640-
    In: Nutrients, MDPI AG, Vol. 15, No. 7 ( 2023-03-28), p. 1640-
    Abstract: Vascular inflammation triggers the development of thoracic aortic dissection (TAD). Zinc deficiency could dampen tissue inflammation. However, the role of zinc as a nutritional intervention in the progression of TAD remains elusive. In this study, we employed a classical β-aminopropionitrile monofumarate (BAPN)-induced TAD model in mice treated with low zinc and observed that the TAD progression was greatly ameliorated under low zinc conditions. Our results showed that low zinc could significantly improve aortic dissection and rupture (BAPN + low zinc vs. BAPN, 36% vs. 100%) and reduce mortality (BAPN + low zinc vs. BAPN, 22% vs. 57%). Mechanically, low zinc attenuated the infiltration of macrophages and inhibited the expression of inflammatory cytokines, suppressed the phenotype switch of vascular smooth muscle cells from contractile to synthetic types, and eventually alleviated the development of TAD. In conclusion, this study suggested that low zinc may serve as a potential nutritional intervention approach for TAD prevention.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2518386-2
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  • 10
    In: The American Journal of Clinical Nutrition, Elsevier BV, Vol. 114, No. 2 ( 2021-08), p. 780-793
    Type of Medium: Online Resource
    ISSN: 0002-9165
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1496439-9
    SSG: 12
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