Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by mitochondrial dynamics imbalance

This study investigated the cardioprotective effect of vitexin against MIRI and its possible mechanism. Isolated SD rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Ex vivo experiments showed improved left ventricular function and reduced infarct size in the vitexin group. Transmission electron microscopy showed that I/R caused outer mitochondrial membrane rupture, cristae disappearance and vacuolation, while vitexin reduced mitochondrial damage and ultimately reduced cardiomyocyte apoptosis. In vitro, vitexin protected H9c2 cells from H/R-induced mitochondrial dysfunction, significantly reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria. These results suggest a new protective mechanism of vitexin for ischemic heart disease treatment.
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research

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In conclusion, T2D impairs vascular function by dysregulated autophagy. Therefore, autophagy could be a potential target for overcoming diabetic microvascular complications. To What Degree Does Loss of Skeletal Muscle with Age Contribute to Immunosenescence? https://www.fightaging.org/archives/2019/11/to-what-degree-does-loss-of-skeletal-muscle-with-age-contribute-to-immunosenescence/ Sarcopenia, the progressive loss of muscle mass and strength, is characteristic of aging. A perhaps surprisingly large fraction of the losses can be averted by strength training, but there are nonetheless inexorable process...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, EMPA can trigger AMPK signaling pathways and modulate myocardial contractility and reduce myocardial infarct size caused by ischemia and reperfusion independent of hypoglycemic effect. The results for the first time demonstrate that the activation of AMPK by EMPA could one reason about EMPA's beneficial effects on heart disease.Graphical abstract
Source: Molecular and Cellular Endocrinology - Category: Endocrinology Source Type: research
In conclusion, TSF improved lipid accumulation and hepatic steatosis by inducing the AMPK/SIRT1 pathway-mediated autophagy. Introduction Nonalcoholic fatty liver disease (NAFLD) has become a worldwide health concern due to the increased incidence of obesity and diabetes. In addition, NAFLD is closely associated with the risk factors of coronary heart disease, such as metabolic syndrome, diabetes mellitus, and dyslipidemia, which are considered to be the leading causes of death (Wiest et al., 2017). Although our understanding of the pathogenesis of NAFLD has significantly improved, there is still no effective medica...
Source: Frontiers in Physiology - Category: Physiology Source Type: research
This study demonstrated that the incidence of ischemic heart disease and death were three times higher among men with low birth weight compared to men with high birth weight (5). Epidemiological investigations of adults born at the time of the Dutch famine between 1944 and 1945 revealed an association between maternal starvation and a low infant birth weight with a high incidence of hypertension and coronary heart disease in these adults (23). Furthermore, Painter et al. reported the incidence of early onset coronary heart disease among persons conceived during the Dutch famine (24). In that regard, Barker's findin...
Source: Frontiers in Endocrinology - Category: Endocrinology Source Type: research
Right ventricular (RV) dysfunction secondary to pulmonary hypertension is responsible for heart failure and death in many clinical settings, including congenital heart disease, chronic thromboembolic pulmonary hypertension, left-sided heart failure, and pulmonary artery hypertension.1 Increase in RV afterload leads to a series of complex changes that initially result in compensatory hypertrophy and increased contractility, followed by RV dilatation and failure.2,3 The mechanisms responsible for these changes include ventriculoarterial uncoupling, myocardial ischemia secondary to decreased perfusion pressure and capillary r...
Source: The Journal of Thoracic and Cardiovascular Surgery - Category: Cardiovascular & Thoracic Surgery Authors: Tags: Commentary Source Type: research
Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more. This content is...
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This study indicates that frailty and other age-related diseases could be prevented and significantly reduced in older adults. Getting our heart risk factors under control could lead to much healthier old ages. Unfortunately, the current obesity epidemic is moving the older population in the wrong direction, however our study underlines how even small reductions in risk are worthwhile." The study analysed data from more than 421,000 people aged 60-69 in both GP medical records and in the UK Biobank research study. Participants were followed up over ten years. The researchers analysed six factors that could impa...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, senescence of vascular cells promotes the development of age-related disorders, including heart failure, diabetes, and atherosclerotic diseases, while suppression of vascular cell senescence ameliorates phenotypic features of aging in various models. Recent findings have indicated that specific depletion of senescent cells reverses age-related changes. Although the biological networks contributing to maintenance of homeostasis are extremely complex, it seems reasonable to explore senolytic agents that can act on specific cellular components or tissues. Several clinical trials of senolytic agents are currentl...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more. This content is...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In this study, we have shown that the lipid chaperones FABP4/FABP5 are critical intermediate factors in the deterioration of metabolic systems during aging. Consistent with their roles in chronic inflammation and insulin resistance in young prediabetic mice, we found that FABPs promote the deterioration of glucose homeostasis; metabolic tissue pathologies, particularly in white and brown adipose tissue and liver; and local and systemic inflammation associated with aging. A systematic approach, including lipidomics and pathway-focused transcript analysis, revealed that calorie restriction (CR) and Fabp4/5 deficiency result ...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
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