• Mashup Score: 4

    Clinical guidelines broadly recommend exercise training for patients with heart failure (HF). This review examines clinical benefits of exercise training across HF subtypes, focusing on clinical trials with key outcomes including mortality, hospitalization, exercise capacity, and quality of life. We also explore physiological and molecular mechanisms by which exercise training may improve HF, including organ-specific effects along the oxygen transport pathway from the cardiopulmonary system to the peripheral vasculature and skeletal muscles. We further review global mechanisms underlying the benefits of exercise training in HF, including antiinflammatory, immunomodulatory, and antioxidative effects, in addition to neurohormonal regulation and interorgan crosstalk. Finally, we identify future research directions to refine and support evidence-based exercise training prescriptions for HF management.

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Exercise Training in #HeartFailure: Clinical Benefits and Mechanisms https://t.co/iwGDLNxYNo Authored by @LouisaMounsey & colleagues @JenHoCardiology @emilyswlau https://t.co/TPVLG1pWYM

  • Mashup Score: 3

    Exercise is generally considered beneficial for cardiovascular health, but for patients with inherited cardiomyopathies, exercise can be a source of anxiety due to concerns about arrhythmia risk and disease progression. In the general population, exercise avoidance can impact cardiometabolic health and diminished fitness is a risk factor for heart failure. At the other extreme, sustained high levels of exercise in competitive endurance athletes have been associated with an increased risk of some arrhythmias. Defining optimal threshold levels for exercise participation is not straightforward and one-size-fits-all recommendations are unlikely to be successful. In the context of inherited cardiomyopathies, the impact of exercise on myocardial function and arrhythmias depends on factors such as exercise frequency, intensity, and duration, as well as the type of cardiomyopathy, underlying genotype, and other unique intrinsic traits in each individual. This review outlines current knowledge

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Exercise in Inherited #Cardiomyopathies: Optimizing the Dose-Response Curve https://t.co/xEeE1XAM8v Authored by @drellerye & colleagues. @FatkinLab @alagerche @celinefsantiago https://t.co/5HIIBjOnFj

  • Mashup Score: 2

    Subjective and objective limitations to exercise and activity are hallmarks of heart failure (HF), regardless of underlying ejection fraction (EF). These limitations relate to cardiovascular abnormalities involving the systolic and diastolic properties of the heart, venous, and arterial vasculature, as well as noncardiovascular abnormalities, including impairments in pulmonary function, autonomic regulation, anemia, metabolism, and changes in mitochondria and skeletal muscle. The contribution of these abnormalities varies between patients with HF with preserved EF and those with HF with reduced EF, but, even within each HF subtype, there is substantial individual patient pathophysiologic variability, which suggests a potentially important role for phenotyping based on exercise reserve responses to individualize treatment. In this article, we review the current understanding of exercise reserve limitation with a focus on specific organ systems involved, both in patients with HF with pre

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Physiologic Phenotyping of Responses to Exercise and Activity in #HeartFailure https://t.co/rYKRP9Wrz1 Authored by @GLewisCardiol & colleagues. @bborlaugmd https://t.co/jPtHkjfkKz

  • Mashup Score: 10

    Regular exercise is widely known to exert beneficial effects on the cardiovascular system. Despite the widely accepted and numerous benefits of exercise, whether there is an upper limit to these benefits is unclear, particularly with regard to atherosclerotic disease. Observational cohort studies over the past 2 decades have identified a consistent signal of increased coronary artery calcification in older men, who have been exposed to high volumes of endurance exercise over their lifetime. The clinical ramifications of these findings are not fully known, as outcomes studies in these athletic populations are needed, but given the strong associations of coronary artery calcification with adverse cardiovascular events, a deeper mechanistic understanding of the link between endurance exercise and coronary artery calcification is needed. In this review, we describe the possible underlying mechanisms that may explain this conundrum of the athlete calcification paradox at the molecular and c

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Paradox of Exercise and Coronary #Artery #Calcification: Potential Underlying Mechanisms https://t.co/KEt6r6h2Zh Authored by @JeffHsuMD & colleagues. @YinTintut https://t.co/HLvYXW8Rwj

  • Mashup Score: 3

    Skeletal muscle is essential for movement and maintaining energy homeostasis and is the primary tissue for insulin-stimulated glucose uptake. Skeletal muscle is composed of various cell types that help to govern the delivery, transport, and metabolism of nutrients to and within the tissue. Dysregulation of these processes can result in impaired insulin-stimulated glucose uptake and dysglycemia—insulin resistance and type 2 diabetes. Acute exercise and chronic exercise training provide a robust stimulus to improve nutrient delivery, nutrient transport into a cell, and subsequent storage and oxidation to help improve insulin sensitivity. This review details the molecular mechanisms of skeletal muscle insulin resistance and how exercise counteracts these defects, highlighting the key role of exercise in muscle health and disease.

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Unraveling Skeletal #Muscle #Insulin Resistance: Molecular Mechanisms and the Restorative Role of Exercise https://t.co/py6BQ9Ocmh Authored by @KatieWhytock & BH Goodpaster https://t.co/fpQW433Grg

  • Mashup Score: 2

    Diabetic cardiomyopathy (DiaCM) is a significant diabetic complication, characterized by abnormal cardiac structure and function without coronary artery disease and hypertension. 1 Regular exercise prevents DiaCM, 2 yet its molecular mechanisms are incompletely understood. N 4-acetylcytidine (ac4C), a posttranscriptional RNA modification catalyzed by the acetyltransferase NAT10 (N -acetyltransferase 10), is implicated in cardiac injuries and heart failure. However, its roles in DiaCM and exercise

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    • @CircRes Compendium on #Cardiopulmonary Disease and #Exercise Shen et al Research Letter "Exercise Mitigates #Diabetic #Cardiomyopathy by Suppressing #Ferroptosis via N-acetyltransferase 10" https://t.co/JhwSIgHQHE @lihabo @sumeetkhetarpal https://t.co/3x2G02ZQs4

  • Mashup Score: 2

    The burden of hypertension is rising rapidly in sub-Saharan Africa (SSA), posing significant health challenges and economic costs that hinder national development. Despite being well-studied in clinical medicine, the detection, treatment, and control of hypertension in SSA remain inadequate. This is due to barriers across the care continuum, including individual-, provider-, and system-level obstacles within the health system. A critical issue is the lack of contextualized mechanistic research to understand the mechanisms, phenotypes, and treatment responses in native SSA populations. Current treatment approaches are often based on data from diaspora Africans, particularly African Americans. Consequently, most guidelines do not recommend angiotensin system drugs as first-line agents for Black patients, a stance that should be reconsidered given some evidence of their effectiveness in native SSA populations. Addressing these barriers requires a comprehensive, multisectoral strategy that

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    • The latest review in the June 20th issue of @CircRes by @ModouJobe et al "#Hypertension in Sub-Saharan #Africa: Burden, Barriers & Priorities for Improving Treatment Outcomes" https://t.co/4r9w4jP5QM @KEMRI_Wellcome @rGayeBamba @dikeojji @SerigneMorBeye @Majigeen345 @LiliGaye https://t.co/xcXwtOO98j

  • Mashup Score: 3

    BACKGROUND: The fatty acid (FA) transporter CD36 (FA translocase/cluster of differentiation 36) is the gatekeeper of cardiac FA metabolism. Preferential localisation of CD36 to the sarcolemma is one of the initiating cellular responses in the development of muscle insulin resistance and in the type 2 diabetic heart. Post-translational S-acylation controls protein trafficking, and in this study we hypothesised that increased CD36 S-acylation may underpin the preferential sarcolemmal localisation of CD36, driving metabolic and contractile dysfunction in diabetes. METHODS: Type 2 diabetes was induced in the rat using high fat diet and a low dose of streptozotocin. Forkhead box O1 (FoxO1) transcriptional regulation of zDHHC4 (zinc finger DHHC-type palmitoyltransferase 4) and subsequent S-acylation of CD36 was assessed using chromatin immunoprecipitation (ChIP) sequencing, ChIP-quantitative polymerase chain reaction, luciferase assays, siRNA (small interfering RNA) and shRNA silencing. RESU

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    • 4/4 @KaitDennis19 et al FoxO1-zDHHC4-CD36 S-Acylation Axis Drives Metabolic Dysfunction in Diabetes https://t.co/e4SEpOR3jq @Heatherlab_ox @JussherLab @FullerLabGlas @dunjaaks @MarcosCG_95 @ujangpurnama_

  • Mashup Score: 8

    BACKGROUND: Preeclampsia is a placenta-origin pregnancy complication. Although its development has long been divided into 2 stages: abnormal placentation (stage I) and the release of factors from the hypoperfused placenta into circulation, triggering preeclampsia due to endothelial dysfunction (stage II), the placenta-derived substances coupling the 2 stages remain unclear. METHODS: Extracellular vesicles (EVs) from normal and preeclampsia-complicated placentas were intravenously administered to pregnant mice, and blood pressure was recorded throughout pregnancy. The differential cargo, including NEP (neprilysin), of placental EVs in normal and preeclamptic placentas was identified by liquid chromatography-mass spectrometry, and the cell types involved in NEP expression in the placenta were determined by single-cell RNA sequencing. The effects of placental EVs and recombinant mouse NEP on the uterine arteries were assessed by myography. Placenta-specific NEP overexpression mice were es

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    • He et al found that #NEP, secreted by trophoblast cells & shuttled to maternal blood vessels through #EVs, is a key culprit behind #pre-eclampsia. Learn more about new research strategies for treating preeclampsia at https://t.co/0IS45y3fWm @mark_D_kilby https://t.co/6YUSBdXKz2