Novel Cardioprotective(新型心脏保护剂)研究综述
Novel Cardioprotective 新型心脏保护剂 - Allyl Methyl Sulfide (AMS) is a novel cardioprotective metabolite identified in the serum of rats after raw garlic administration. [1] Conclusion: Oral administration of ketotifen appears to be efficient and safe as a novel cardioprotective agent for the prevention of anthracyclines induced cardiotoxicity. [2] CONCLUSIONS: This study unveils novel cardioprotective effects of RvD1 in angiotensin II-induced hypertension and cardiac remodeling by attenuating inflammation and provides insights into a potential clinical application. [3] To address this, we propose an in vivo set of step-by-step criteria for IM proving P reclinical A ssessment of C ardioprotective T herapies (‘IMPACT’), for investigators to consider adopting before embarking on clinical studies, the aim of which is to improve the likelihood of translating novel cardioprotective interventions into the clinical setting for patient benefit. [4] CONCLUSION We show that, in addition to its anti-oxidant and anti-apoptotic effects, hydralazine, confers acute cardioprotection by inhibiting IRI-induced mitochondrial fission, raising the possibility of repurposing hydralazine as a novel cardioprotective therapy for improving post-infarction outcomes. [5] Here, we review current putative risk genes and variants, the strength of evidence for each genetic association and the interaction between risk genes, in the context of known clinical risk factors and potential novel cardioprotective strategies. [6] METHODS AND RESULTS In mice lacking Ffar4 (Ffar4KO), we found that Ffar4 is required for an adaptive response to pressure overload induced by transverse aortic constriction (TAC), identifying a novel cardioprotective function for Ffar4. [7] This review aimed to summarize existing evidence supporting targeting of Lp(a) as a novel cardioprotective strategy. [8] We identified a novel cardioprotective E2-ERα-BMPR2-apelin axis in the RV. [9] IOE exhibited a novel cardioprotective effect, as shown by improvement in cardiac function and decrease in infarct size. [10] Conclusion: Oral administration of ketotifen appears to be efficient and safe as a novel cardioprotective agent for the prevention of anthracyclines induced cardiotoxicity. [11] The toxic mechanisms of many anticancer drugs have been revealed, but more studying and understanding of the mechanisms of drug-induced mitochondrial toxicity is required to develop mitochondrial toxicity screening system as well as novel cardioprotective strategies for the prevention of cardiac disorders of drugs. [12] These in vitro and in vivo results point towards the fact that CN might be a novel cardioprotective agent against DOX-induced cardiotoxicity through modulating cardio apoptosis and oxidative stress. [13] By revealing specific changes in preferential binding partners of the BAG3C151R protein variant, we also identify potential targets for the development of novel cardioprotective therapies. [14] These results reinforce the importance of carefully evaluating the PGC1α-boosting strategies in a context-dependent manner to facilitate clinical translation of novel cardioprotective therapies. [15] Diosgenin and Ginsenoside Re could be helpful to find the lead compounds on designing and developing novel cardioprotective agents. [16] In this manuscript we provide a detailed protocol closely mimicking current clinical practices in the context of DCD with continuous monitoring of heart function, allowing for the evaluation of novel cardioprotective strategies and interventions to decrease ischemia-reperfusion injury. [17] This study reveals MLK3-JNK signaling as a novel cardioprotective signaling axis in the setting of pressure overload. [18] Altogether, our results identify MKP1 as a novel cardioprotective factor in TNF‐α‐related septic cardiomyopathy via affecting mitochondrial division by the way of JNK–MIEF1 signaling pathway. [19] Finally, we will review novel cardioprotective targets translatable to surgical patients. [20] Results In Ffar4KO mice, TAC induced more severe remodeling, identifying an entirely novel cardioprotective role for Ffar4 in the heart. [21] This study supplied valuable information to develop novel cardioprotective agents from NP extract. [22] Conclusions Our study, performed both in vivo and in vitro, delineates a novel cardioprotective signalling pathway activated by HDL, involving STAT3-mediated decrease of miR-34b and miR-337 expression. [23] CONCLUSION The obtained results may help to guide the further pre-clinical research of LS-102 as a potentially novel cardioprotective agent. [24] Housing mice under daylight conditions prior to myocardial ischemia and reperfusion (IR)-injury, uncovered circadian PER2 amplitude enhancement as novel cardioprotective strategy, mimicking HIF1A metabolic adaptation to myocardial ischemia in a PER2 regulated manner. [25] This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model. [26] Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling. [27] We sought to determine if extended cold storage was possible for DCD hearts following NRP and to compare hearts stored using standard cold storage with a novel cardioprotective solution designed for room temperature storage. [28] Transcriptome analysis revealed that, among 15 genes significantly downregulated (MI+CIH versus MI), Ctrp9 (a novel cardioprotective cardiokine) was one of the most significantly inhibited genes. [29] Our results concerning the potent antithrombotic effects of FGE-salmon-PLs against both PAF and thrombin pathways strongly suggest that such food-grade extracts are putative candidates for the development of novel cardioprotective supplements and nutraceuticals. [30] Thus, this study demonstrates that 63 and TR002 represent novel cardioprotective agents that inhibit PTP opening independent of CyPD targeting. [31] This model represents a new preclinical platform for studying cardiac ischemia with human cells, which does not rely on biomarker analysis and has the potential for screening novel cardioprotective drugs with readouts that are closer to the measured clinical parameters. [32] Further studies are vital to identify the hormone responsible for activating pro-survival pathways but our data highlights the potential use of SGLT2 inhibitors as a novel cardioprotective therapy in high-risk cardiovascular patients regardless of diabetic status. [33] This work highlights the novel cardioprotective effect of vitamin D3 in the experimental model of HFD feeding through the downregulation of UCP3. [34] Here, we describe a pre-clinical large-animal (porcine) model of orthotopic heart transplantation that has been firmly established and previously used to investigate novel cardioprotective strategies. [35] Interleukin (IL)-33/ST2L signaling is a novel cardioprotective pathway, which is antagonized by the soluble isoform sST2. [36] Our previous studies have revealed that astaxanthin (ATX) exhibits novel cardioprotective activity against Hcy-induced cardiotoxicity in vitro and in vivo. [37] These biomarkers may help identify patients for novel cardioprotective anti-hyperglycemics, even in the absence of pre-existing CVD. [38]烯丙基甲基硫醚 (AMS) 是一种新型的心脏保护代谢物，在给予生大蒜后大鼠血清中发现。 [1] 结论：口服酮替芬作为预防蒽环类药物诱导的心脏毒性的新型心脏保护剂似乎是有效和安全的。 [2] 结论：本研究通过减轻炎症揭示了 RvD1 在血管紧张素 II 诱导的高血压和心脏重塑中的新型心脏保护作用，并为潜在的临床应用提供了见解。 [3] 为了解决这个问题，我们提出了一套体内循序渐进的标准，用于 IM 证明心脏保护疗法的临床前评估（“IMPACT”），供研究人员在开始临床研究之前考虑采用，其目的是是提高将新型心脏保护干预措施转化为临床环境以使患者受益的可能性。 [4] 结论 我们表明，除了其抗氧化和抗凋亡作用外，肼苯哒嗪通过抑制 IRI 诱导的线粒体裂变赋予急性心脏保护作用，提高了将肼苯哒嗪重新用作改善梗死后预后的新型心脏保护疗法的可能性。 [5] 在这里，我们在已知的临床风险因素和潜在的新型心脏保护策略的背景下，回顾了当前推定的风险基因和变异、每种遗传关联的证据强度以及风险基因之间的相互作用。 [6] 方法和结果 在缺乏 Ffar4 (Ffar4KO) 的小鼠中，我们发现 Ffar4 是对横向主动脉缩窄 (TAC) 引起的压力过载的适应性反应所必需的，从而确定了 Ffar4 的一种新的心脏保护功能。 [7] 本综述旨在总结支持靶向 Lp(a) 作为一种新型心脏保护策略的现有证据。 [8] 我们在 RV 中发现了一种新型的心脏保护 E2-ERα-BMPR2-apelin 轴。 [9] IOE 表现出一种新的心脏保护作用，如心脏功能的改善和梗塞面积的减少所示。 [10] 结论：口服酮替芬作为预防蒽环类药物诱导的心脏毒性的新型心脏保护剂似乎是有效和安全的。 [11] 许多抗癌药物的毒性机制已被揭示，但需要更多地研究和了解药物诱导的线粒体毒性机制，以开发线粒体毒性筛选系统以及预防药物心脏疾病的新型心脏保护策略。 [12] 这些体外和体内结果表明，CN 可能是一种通过调节心脏细胞凋亡和氧化应激来对抗 DOX 诱导的心脏毒性的新型心脏保护剂。 [13] 通过揭示 BAG3C151R 蛋白变体的优先结合伙伴的特定变化，我们还确定了开发新型心脏保护疗法的潜在目标。 [14] 这些结果强调了以上下文相关的方式仔细评估 PGC1α 增强策略以促进新型心脏保护疗法的临床转化的重要性。 [15] 薯蓣皂苷元和人参皂苷 Re 有助于寻找设计和开发新型心脏保护剂的先导化合物。 [16] 在这份手稿中，我们提供了一个详细的协议，在 DCD 的背景下密切模仿当前的临床实践，并持续监测心脏功能，从而可以评估新的心脏保护策略和干预措施以减少缺血再灌注损伤。 [17] 这项研究揭示了 MLK3-JNK 信号传导作为压力超负荷设置中的一种新型心脏保护信号轴。 [18] 总之，我们的结果通过 JNK-MIEF1 信号通路影响线粒体分裂，将 MKP1 确定为 TNF-α 相关脓毒性心肌病的新型心脏保护因子。 [19] 最后，我们将回顾可转化为手术患者的新型心脏保护靶点。 [20] 结果 在 Ffar4KO 小鼠中，TAC 诱导了更严重的重塑，确定了 Ffar4 在心脏中的全新心脏保护作用。 [21] 这项研究为从 NP 提取物中开发新型心脏保护剂提供了有价值的信息。 [22] 结论 我们在体内和体外进行的研究描绘了一种由 HDL 激活的新型心脏保护信号通路，包括 STAT3 介导的 miR-34b 和 miR-337 表达的降低。 [23] 结论 获得的结果可能有助于指导 LS-102 作为一种潜在的新型心脏保护剂的进一步临床前研究。 [24] 在心肌缺血和再灌注 (IR) 损伤之前将小鼠置于日光条件下，发现昼夜节律 PER2 振幅增强是一种新的心脏保护策略，以 PER2 调节的方式模拟 HIF1A 对心肌缺血的代谢适应。 [25] 这种使用暴露于 MI-R 的高胆固醇血症 APOE*3-Leiden 小鼠的实验模型似乎适合在临床相关的动物模型中研究新型心脏保护疗法。 [26] 我们的研究揭示了 PN 通过 Nrf2/HO-1 信号传导对 IMI 大鼠的新型心脏保护作用。 [27] 我们试图确定 NRP 后 DCD 心脏是否可以延长冷藏，并将使用标准冷藏储存的心脏与设计用于室温储存的新型心脏保护解决方案进行比较。 [28] 转录组分析显示，在 15 个显着下调的基因中（MI+CIH 与 MI），Ctrp9（一种新型的心脏保护性心脏因子）是最显着抑制的基因之一。 [29] 我们关于 FGE-salmon-PLs 对 PAF 和凝血酶途径的有效抗血栓作用的结果强烈表明，这种食品级提取物是开发新型心脏保护补充剂和保健品的推定候选者。 [30] 因此，这项研究表明，63 和 TR002 代表了新的心脏保护剂，它们抑制 PTP 开放而不依赖于 CyPD 靶向。 [31] 该模型代表了一个新的临床前平台，用于研究人体细胞的心脏缺血，它不依赖于生物标志物分析，并且有可能筛选出读数更接近于测量的临床参数的新型心脏保护药物。 [32] 进一步的研究对于确定负责激活促生存途径的激素至关重要，但我们的数据强调了 SGLT2 抑制剂作为高危心血管患者的新型心脏保护疗法的潜在用途，无论糖尿病状态如何。 [33] 这项工作通过下调 UCP3 突出了维生素 D3 在 HFD 喂养实验模型中的新型心脏保护作用。 [34] 在这里，我们描述了一种临床前大型动物（猪）原位心脏移植模型，该模型已经牢固建立并以前用于研究新的心脏保护策略。 [35] 白细胞介素 (IL)-33/ST2L 信号传导是一种新的心脏保护途径，可被可溶性异构体 sST2 拮抗。 [36] 我们之前的研究表明，虾青素 (ATX) 在体外和体内对 Hcy 诱导的心脏毒性表现出新的心脏保护活性。 [37] 即使没有预先存在的心血管疾病，这些生物标志物也可能有助于识别具有新型心脏保护性抗高血糖药的患者。 [38]
novel cardioprotective agent 新型心脏保护剂
Conclusion: Oral administration of ketotifen appears to be efficient and safe as a novel cardioprotective agent for the prevention of anthracyclines induced cardiotoxicity. [1] Conclusion: Oral administration of ketotifen appears to be efficient and safe as a novel cardioprotective agent for the prevention of anthracyclines induced cardiotoxicity. [2] These in vitro and in vivo results point towards the fact that CN might be a novel cardioprotective agent against DOX-induced cardiotoxicity through modulating cardio apoptosis and oxidative stress. [3] Diosgenin and Ginsenoside Re could be helpful to find the lead compounds on designing and developing novel cardioprotective agents. [4] This study supplied valuable information to develop novel cardioprotective agents from NP extract. [5] CONCLUSION The obtained results may help to guide the further pre-clinical research of LS-102 as a potentially novel cardioprotective agent. [6] Thus, this study demonstrates that 63 and TR002 represent novel cardioprotective agents that inhibit PTP opening independent of CyPD targeting. [7]结论：口服酮替芬作为预防蒽环类药物诱导的心脏毒性的新型心脏保护剂似乎是有效和安全的。 [1] 结论：口服酮替芬作为预防蒽环类药物诱导的心脏毒性的新型心脏保护剂似乎是有效和安全的。 [2] 这些体外和体内结果表明，CN 可能是一种通过调节心脏细胞凋亡和氧化应激来对抗 DOX 诱导的心脏毒性的新型心脏保护剂。 [3] 薯蓣皂苷元和人参皂苷 Re 有助于寻找设计和开发新型心脏保护剂的先导化合物。 [4] 这项研究为从 NP 提取物中开发新型心脏保护剂提供了有价值的信息。 [5] 结论 获得的结果可能有助于指导 LS-102 作为一种潜在的新型心脏保护剂的进一步临床前研究。 [6] 因此，这项研究表明，63 和 TR002 代表了新的心脏保护剂，它们抑制 PTP 开放而不依赖于 CyPD 靶向。 [7]
novel cardioprotective strategy 新的心脏保护策略
Here, we review current putative risk genes and variants, the strength of evidence for each genetic association and the interaction between risk genes, in the context of known clinical risk factors and potential novel cardioprotective strategies. [1] This review aimed to summarize existing evidence supporting targeting of Lp(a) as a novel cardioprotective strategy. [2] The toxic mechanisms of many anticancer drugs have been revealed, but more studying and understanding of the mechanisms of drug-induced mitochondrial toxicity is required to develop mitochondrial toxicity screening system as well as novel cardioprotective strategies for the prevention of cardiac disorders of drugs. [3] In this manuscript we provide a detailed protocol closely mimicking current clinical practices in the context of DCD with continuous monitoring of heart function, allowing for the evaluation of novel cardioprotective strategies and interventions to decrease ischemia-reperfusion injury. [4] Housing mice under daylight conditions prior to myocardial ischemia and reperfusion (IR)-injury, uncovered circadian PER2 amplitude enhancement as novel cardioprotective strategy, mimicking HIF1A metabolic adaptation to myocardial ischemia in a PER2 regulated manner. [5] Here, we describe a pre-clinical large-animal (porcine) model of orthotopic heart transplantation that has been firmly established and previously used to investigate novel cardioprotective strategies. [6]在这里，我们在已知的临床风险因素和潜在的新型心脏保护策略的背景下，回顾了当前推定的风险基因和变异、每种遗传关联的证据强度以及风险基因之间的相互作用。 [1] 本综述旨在总结支持靶向 Lp(a) 作为一种新型心脏保护策略的现有证据。 [2] 许多抗癌药物的毒性机制已被揭示，但需要更多地研究和了解药物诱导的线粒体毒性机制，以开发线粒体毒性筛选系统以及预防药物心脏疾病的新型心脏保护策略。 [3] 在这份手稿中，我们提供了一个详细的协议，在 DCD 的背景下密切模仿当前的临床实践，并持续监测心脏功能，从而可以评估新的心脏保护策略和干预措施以减少缺血再灌注损伤。 [4] 在心肌缺血和再灌注 (IR) 损伤之前将小鼠置于日光条件下，发现昼夜节律 PER2 振幅增强是一种新的心脏保护策略，以 PER2 调节的方式模拟 HIF1A 对心肌缺血的代谢适应。 [5] 在这里，我们描述了一种临床前大型动物（猪）原位心脏移植模型，该模型已经牢固建立并以前用于研究新的心脏保护策略。 [6]
novel cardioprotective therapy 新型心脏保护疗法
CONCLUSION We show that, in addition to its anti-oxidant and anti-apoptotic effects, hydralazine, confers acute cardioprotection by inhibiting IRI-induced mitochondrial fission, raising the possibility of repurposing hydralazine as a novel cardioprotective therapy for improving post-infarction outcomes. [1] By revealing specific changes in preferential binding partners of the BAG3C151R protein variant, we also identify potential targets for the development of novel cardioprotective therapies. [2] These results reinforce the importance of carefully evaluating the PGC1α-boosting strategies in a context-dependent manner to facilitate clinical translation of novel cardioprotective therapies. [3] This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model. [4] Further studies are vital to identify the hormone responsible for activating pro-survival pathways but our data highlights the potential use of SGLT2 inhibitors as a novel cardioprotective therapy in high-risk cardiovascular patients regardless of diabetic status. [5]结论 我们表明，除了其抗氧化和抗凋亡作用外，肼苯哒嗪通过抑制 IRI 诱导的线粒体裂变赋予急性心脏保护作用，提高了将肼苯哒嗪重新用作改善梗死后预后的新型心脏保护疗法的可能性。 [1] 通过揭示 BAG3C151R 蛋白变体的优先结合伙伴的特定变化，我们还确定了开发新型心脏保护疗法的潜在目标。 [2] 这些结果强调了以上下文相关的方式仔细评估 PGC1α 增强策略以促进新型心脏保护疗法的临床转化的重要性。 [3] 这种使用暴露于 MI-R 的高胆固醇血症 APOE*3-Leiden 小鼠的实验模型似乎适合在临床相关的动物模型中研究新型心脏保护疗法。 [4] 进一步的研究对于确定负责激活促生存途径的激素至关重要，但我们的数据强调了 SGLT2 抑制剂作为高危心血管患者的新型心脏保护疗法的潜在用途，无论糖尿病状态如何。 [5]
novel cardioprotective effect 新的心脏保护作用
CONCLUSIONS: This study unveils novel cardioprotective effects of RvD1 in angiotensin II-induced hypertension and cardiac remodeling by attenuating inflammation and provides insights into a potential clinical application. [1] IOE exhibited a novel cardioprotective effect, as shown by improvement in cardiac function and decrease in infarct size. [2] Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling. [3] This work highlights the novel cardioprotective effect of vitamin D3 in the experimental model of HFD feeding through the downregulation of UCP3. [4]结论：本研究通过减轻炎症揭示了 RvD1 在血管紧张素 II 诱导的高血压和心脏重塑中的新型心脏保护作用，并为潜在的临床应用提供了见解。 [1] IOE 表现出一种新的心脏保护作用，如心脏功能的改善和梗塞面积的减少所示。 [2] 我们的研究揭示了 PN 通过 Nrf2/HO-1 信号传导对 IMI 大鼠的新型心脏保护作用。 [3] 这项工作通过下调 UCP3 突出了维生素 D3 在 HFD 喂养实验模型中的新型心脏保护作用。 [4]