UNASSIGNED: This systematic review investigates the interplay between oxytocin and exercise; in terms of analgesic, anti-inflammatory, pro-regenerative, and cardioprotective effects. Furthermore, by analyzing measurement methods, we aim to improve measurement validity and reliability.
UNASSIGNED: Utilizing PRISMA, GRADE, and MECIR protocols, we examined five databases with a modified SPIDER search. Including studies on healthy participants, published within the last 20 years, based on keywords \"oxytocin,\" \"exercise\" and \"measurement,\" 690 studies were retrieved initially (455 unique records). After excluding studies of clinically identifiable diseases, and unpublished and reproduction-focused studies, 175 studies qualified for the narrative cross-thematic and structural analysis.
UNASSIGNED: The analysis resulted in five categories showing the reciprocal impact of oxytocin and exercise: Exercise (50), Physiology (63), Environment (27), Social Context (65), and Stress (49). Exercise-induced oxytocin could promote tissue regeneration, with 32 studies showing its analgesic and anti-inflammatory effects, while 14 studies discussed memory and cognition. Furthermore, empathy-associated OXTR rs53576 polymorphism might influence team sports performance. Since dietary habits and substance abuse can impact oxytocin secretion too, combining self-report tests and repeated salivary measurements may help achieve precision.
UNASSIGNED: Oxytocin\'s effect on fear extinction and social cognition might generate strategies for mental training, and technical, and tactical development in sports. Exercise-induced oxytocin can affect the amount of stress experienced by athletes, and their response to it. However, oxytocin levels could depend on the type of sport in means of contact level, exercise intensity, and duration. The influence of oxytocin on athletes\' performance and recovery could have been exploited due to its short half-life. Examining oxytocin\'s complex interactions with exercise paves the way for future research and application in sports science, psychology, and medical disciplines.
UNASSIGNED: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=512184, identifier CRD42024512184.

Doxorubicin (DOX), a cornerstone of cancer chemotherapy, is marred by its dose-dependent cardiotoxicity, leading to cardiomyopathy and heart failure. The epidemiology of DOX-related cardiotoxicity highlights its cumulative, progressive nature, with a significant impact on the health of patients. The pathophysiological mechanisms involve mitochondrial dysfunction, oxidative stress and disrupted calcium homeostasis in cardiomyocytes. Despite the search for effective cardioprotective strategies, current treatments offer limited efficacy. Visnagin emerges as a potential solution, known for its vasodilatory and anti-inflammatory properties, and recent studies suggest its cardioprotective efficacy against DOX-induced cardiotoxicity through mitochondrial protection, the modulation of key signaling pathways and the inhibition of apoptosis. The present review aimed to provide a comprehensive overview of the mechanisms of action of visnagin, as well as to provide experimental evidence, and potential integration into cancer treatment regimens, highlighting its promise as a novel therapeutic agent for managing cardiotoxicity in patients undergoing anthracycline chemotherapy.

The cardiovascular system is mainly responsible for the transport of substances necessary to cellular metabolism. However, for the good performance of this function, there is need for adequate control of blood pressure levels of tissue perfusion and systemic arterial. Acute myocardial infarction is one of the complications of the cardiovascular system, that most affects the population around the world. This condition can be defined as a disease generated by an imbalance of oxygen concentrations used in cardiovascular metabolism, this change usually occurs because coronary occlusion, which prevents myocardial blood flow. The diagnosis is based on the set of clinical and laboratory investigations, which are in the release of cardiac enzyme biomarkers, cardiovascular and hemodynamic changes and cardiac accommodations. The treatment consists in the use of concomitant cardiovascular drugs, such as: antihypertensive, antiplatelet and hypolipidemic. Despite improvements in clinical and pharmacological management, acute myocardial infarction remains the leading cause of death worldwide. This finding encourages the scientific research of new drugs for the treatment of myocardial infarction or supporting therapies aimed at reducing the levels of deaths and comorbities generated by cardiovascular diseases.

Ischemic heart disease (IHD) is the leading cause of mortality worldwide and can be complicated by myocardial infarction (MI), leading to cardiac failure. Inorganic nitrite and nitrate, which release nitric oxide (NO), can protect the heart against myocardial injury. This animal systematic review and meta-analysis aims to assess whether the administration of nitrite/nitrate decreases myocardial infarct size. We systematically searched PubMed, Scopus, and Web of Science databases until October 2023; 15 eligible animal studies (35 study arms for in-vivo and 10 for in-vitro studies) published between 1989 and 2023 were included. In-vivo studies were conducted on rats, mice, cats, and dogs, and in-vitro studies on rats and mice with an overall exposure of 0.03 to 12713 mg/kg to nitrate/nitrite administrated before, after, or during ischemia mainly by intravenous single bolus or by oral over 270 days. All in-vitro studies used nitrite/nitrate before ischemia, with the concentration ranging between 0.34 to 201 μM. MI was induced by occlusion of the left anterior diagonal or left circumflex arteries in in-vitro studies and by isoproterenol in in-vivo studies. Infarct size was measured by direct staining of the sliced heart sections. In in-vivo studies, nitrite (overall effect size (ES)=-17.0 %, 95 % confidence interval (CI)=-21.3, -12.8, P<0.001) and nitrate (overall ES= -9.6 %, 95 % CI=-15.7, -3.4, P=0.002) reduced myocardial infarct size. In in-vitro studies, nitrite (overall ES=-15.8 %, 95 % CI=-25.5, -6.2, P=0.001) reduced the infarct size. Sensitivity analysis showed that the overall effect of nitrite on myocardial infarct size was unaffected by doses or health conditions in in-vivo and in-vitro studies. In conclusion, our meta-analysis showed that nitrite/nitrate administration can effectively reduce myocardial infarct size. However, these results should be approached with caution because of the limitations of animal studies and the existing high heterogeneity.

Cardiovascular diseases represent a significant worldwide problem, jeopardizing individuals\' physical and mental wellbeing as well as their quality of life as a result of their widespread incidence and fatality. With the aging society, the occurrence of Cardiovascular diseases is progressively rising each year. However, although drugs developed for treating Cardiovascular diseases have clear targets and proven efficacy, they still carry certain toxic and side effect risks. Therefore, finding safe, effective, and practical treatment options is crucial. Scutellarin is the primary constituent of Erigeron breviscapus (Vant.) Hand-Mazz. This article aims to establish a theoretical foundation for the creation and use of secure, productive, and logical medications for Scutellarin in curing heart-related illnesses. Additionally, the examination and analysis of the signal pathway and its associated mechanisms with regard to the employment of SCU in treating heart diseases will impart innovative resolving concepts for the treatment and prevention of Cardiovascular diseases.

Aims: Myocardial ischemia-reperfusion (I/R) injury markedly undermines the protective benefits of revascularization, contributing to ventricular dysfunction and mortality. Due to complex mechanisms, no efficient ways exist to prevent cardiomyocyte reperfusion damage. Vagus nerve stimulation (VNS) appears as a potential therapeutic intervention to alleviate myocardial I/R injury. Hence, this meta-analysis intends to elucidate the potential cellular and molecular mechanisms underpinning the beneficial impact of VNS, along with its prospective clinical implications. Methods and Results: A literature search of MEDLINE, PubMed, Embase, and Cochrane Database yielded 10 articles that satisfied the inclusion criteria. VNS was significantly correlated with a reduced infarct size following myocardial I/R injury [Weighed mean difference (WMD): 25.24, 95% confidence interval (CI): 32.24 to 18.23, p < 0.001] when compared to the control group. Despite high heterogeneity (I2 = 95.3%, p < 0.001), sensitivity and subgroup analyses corroborated the robust efficacy of VNS in limiting infarct expansion. Moreover, meta-regression failed to identify significant influences of pre-specified covariates (i.e., stimulation type or site, VNS duration, condition, and species) on the primary estimates. Notably, VNS considerably impeded ventricular remodeling and cardiac dysfunction, as evidenced by improved left ventricular ejection fraction (LVEF) (WMD: 10.12, 95% CI: 4.28; 15.97, p = 0.001) and end-diastolic pressure (EDP) (WMD: 5.79, 95% CI: 9.84; -1.74, p = 0.005) during the reperfusion phase. Conclusion: VNS offers a protective role against myocardial I/R injury and emerges as a promising therapeutic strategy for future clinical application.

UNASSIGNED: Recently, attention has been paid to the protective properties of active ingredients in Salvia miltiorrhiza (AISM) against organ toxicity induced by chemotherapy drugs. Purpose of the present systematic review is to evaluate the chemoprotective effects and mechanisms of AISM on in vitro and in vivo models of doxorubicin-induced cardiotoxicity (DIC).
UNASSIGNED: According to the PRISMA guideline, the current systematic review was conducted in the Web of Science, PubMed, Embase, and the Cochrane Library to collect all relevant in vitro and in vivo studies on \"the role of AISM on DIC\" published up until May 2023. The SYRCLE\'s tool was used to identify potential risk of bias.
UNASSIGNED: Twenty-two eligible articles were included in this systematic review. Eleven types of active ingredients in Salvia miltiorrhiza were used for DIC, which have the following effects: improvement of physical signs and biochemical indicators, reduction of cardiac function damage caused by DIC, protection of heart tissue structure, enhancement of myocardial cell viability, prevention of cardiomyocyte apoptosis, increase of the chemosensitivity of cancer cells to Doxorubicin, etc. The cardioprotective mechanism of AISM involves inhibiting apoptosis, attenuating oxidative stress, suppressing endoplasmic reticulum (ER) stress, decreasing inflammation, improving mitochondrial structure and function, affecting cellular autophagy and calcium homeostasis. The quality scores of included studies ranged from 4 to 7 points (a total of 10 points), according to SYRCLE\'s risk of bias tool.
UNASSIGNED: This systematic review demonstrated that AISM have chemoprotective effects on DIC in vivo and in vitro models through several main mechanisms such as anti-apoptosis, antioxidant effects, anti-ER stress, and anti-inflammatory.

Dexmedetomidine (DEX), a highly selective alpha2-adrenoceptors agonist, is not only a sedative drug used during mechanical ventilation in the intensive care unit but also a cardio-protective drug against ischemia-reperfusion injury (IRI). Numerous preclinical in vivo and ex vivo studies, mostly evaluating the effect of DEX pretreatment in healthy rodents, have shown the efficacy of DEX in protecting the hearts from IRI. However, whether DEX can maintain its cardio-protective effect in hearts with comorbidities such as diabetes has not been fully elucidated. Multiple clinical trials have reported promising results, showing that pretreatment with DEX can attenuate cardiac damage in patients undergoing cardiac surgery. However, evidence of the post-treatment effects of DEX in clinical practice remains limited. In this narrative review, we summarize the previously reported evidence of DEX-induced cardio-protection against IRI and clarify the condition of the hearts and the timing of DEX administration that has not been tested. With further investigations evaluating these knowledge gaps, the use of DEX as a cardio-protective drug could be further facilitated in the management of patients undergoing cardiac surgery and might be considered in a broader area of clinical settings beyond cardiac surgery, including patients with acute myocardial infarction.

It has been reported that death related to cardiovascular disease has increased up to 12.5% just in the past decade alone with various factors playing a role. In 2015 alone, it has been estimated that there were 422.7 million cases of CVD with 17.9 million deaths. Various therapies have been discovered to control and treat CVDs and their complications including reperfusion therapies and pharmacological approaches but many patients still progress to heart failure. Due to these proven adverse effects of existing therapies, various novel therapeutic techniques have emerged in the near past. Nano formulation is one of them. It is a practical therapeutic strategy to minimize pharmacological therapy\'s side effects and nontargeted distribution. Nanomaterials are suitable for treating CVDs due to their small size, which enables them to reach more sites of the heart and arteries. The biological safety, bioavailability, and solubility of the drugs have been increased due to the encapsulation of natural products and their derivatives of drugs.

Mechanisms contributing to the pathogenesis of myocardial ischemia-reperfusion (I/R) injury are complex and multifactorial. Many strategies have been developed to ameliorate myocardial I/R injuries based on these mechanisms. However, the cardioprotective effects of these strategies appear to diminish in diabetic states. Diabetes weakens myocardial responses to therapies by disrupting intracellular signaling pathways which may be responsible for enhancing cellular resistance to damage. Intriguingly, it was found that Dexmedetomidine (DEX), a potent and selective α2-adrenergic agonist, appears to have the property to reverse diabetes-related inhibition of most intervention-mediated myocardial protection and exert a protective effect. Several mechanisms were revealed to be involved in DEX\'s protection in diabetic rodent myocardial I/R models, including PI3K/Akt and associated GSK-3β pathway stimulation, endoplasmic reticulum stress (ERS) alleviation, and apoptosis inhibition. In addition, DEX could attenuate diabetic myocardial I/R injury by up-regulating autophagy, reducing ROS production, and inhibiting the inflammatory response through HMGB1 pathways. The regulation of autonomic nervous function also appeared to be involved in the protective mechanisms of DEX. In the present review, the evidence and underlying mechanisms of DEX in ameliorating myocardial I/R injury in diabetes are summarized, and the potential of DEX for the treatment/prevention of myocardial I/R injury in diabetic patients is discussed.