Sarcopenia: recent advances for detection, progression, and metabolic alterations along with therapeutic targets.

Sarcopenia, a disorder marked by muscle loss and dysfunction, is a global health concern, particularly in aging populations. Sarcopenia is intricately related to various health conditions, including obesity, dysphagia, and frailty, which underscores the complexity. Despite recent advances in metabolomics and other omics data for early detection and treatment, the precise characterization and diagnosis of sarcopenia remains challenging.

P7C3 ameliorates barium chloride-induced skeletal muscle injury activating transcriptomic and epigenetic modulation of myogenic regulatory factors.

Skeletal muscle injury affects the quality of life in many pathologies, including volumetric muscle loss, contusion injury, and aging. We hypothesized that the nicotinamide phosphoribosyltransferase (Nampt) activator P7C3 improves muscle repair following injury. In the present study, we tested the effect of P7C3 (1-anilino-3-(3,6-dibromocarbazol-9-yl) propan-2-ol) on chemically induced muscle injury.

Combined Endurance and Resistance Exercise Mitigates Age-Associated Cardiac Dysfunction.

Aging is associated with a decline in cardiac function. Exercise has been shown to effectively reduce the risks of cardiovascular diseases. Here whether a combination of endurance and resistance exercises can improve cardiac function in aged mice during late life is investigated.

Exercise reduces pro-inflammatory lipids and preserves resolution mediators that calibrate macrophage-centric immune metabolism in spleen and heart following obesogenic diet in aging mice.

The study investigated the role of volunteer exercise and an obesogenic diet (OBD) in mice, focusing on the splenocardiac axis and inflammation-resolution signaling. Male C57BL/6J mice (2 months old) were assigned to control (CON) or OBD groups for ten months, then randomized into sedentary (Sed) or exercise (Exe) groups for two weeks. Leukocytes, heart function, structure, and spleen tissue examined for inflammation-resolution mediators and macrophage-centric gene transcripts.

Muscle-Brain crosstalk in cognitive impairment.

Sarcopenia is an age-related, involuntary loss of skeletal muscle mass and strength. Alzheimer's disease (AD) is the most common cause of dementia in elderly adults. To date, no effective cures for sarcopenia and AD are available.

Transformational Applications of Human Cardiac Organoids in Cardiovascular Diseases.

Organoid technology has significantly advanced in recent years and revolutionized the field for generation of organs using systems (a.k.a "organs in a dish").

Cardioprotective Effects of 1-(3,6-Dibromo-carbazol-9-yl)-3-Phenylamino-Propan-2-Ol in Diabetic Hearts via Nicotinamide Phosphoribosyltransferase Activation.

Diabetes is associated with increased cardiac injury and sudden death. Nicotinamide phosphoribosyltransferase (Nampt) is an essential enzyme for the NAD salvage pathway and is dysregulated in diabetes. Nampt activation results in rescued NADH/NAD ratios and provides pharmacological changes necessary for diabetic cardioprotection.

CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome.

The prognosis of cardiorenal dysfunction induced by diabetes mellitus (DM), which belongs to cardiorenal syndrome type 5, is poor and its pathogenesis remains elusive. We have reported that CX3CL1 exacerbated heart failure and direct inhibition of CX3CL1 improved cardiac function. Emerging evidence supports that CX3CL1 is involved in renal impairment.

Deep learning based fully automatic segmentation of the left ventricular endocardium and epicardium from cardiac cine MRI.

Background: The segmentation of cardiac medical images is a crucial step for calculating clinical indices such as wall thickness, ventricular volume, and ejection fraction.

Methods: In this study, we introduce a method named LsUnet that combines multi-channel, fully convolutional neural network, and annular shape level-set methods for efficiently segmenting cardiac cine magnetic resonance (MR) images. In this method, the multi-channel deep learning algorithm is applied to train the segmentation task to extract the left ventricle (LV) endocardial and epicardial contours.

Cell-modified bioprinted microspheres for vascular regeneration.

Cell therapy is a promising strategy in which living cells or cellular materials are delivered to treat a variety of diseases. Here, we developed an electrospray bioprinting method to rapidly generate cell-laden hydrogel microspheres, which limit the migration of the captured cells and provide an immunologically privileged microenvironment for cell survival in vivo. Currently, therapeutic angiogenesis aims to induce collateral vessel formation after limb ischemia.

Extracellular Vesicles From Notch Activated Cardiac Mesenchymal Stem Cells Promote Myocyte Proliferation and Neovasculogenesis.

Cardiac mesenchymal stem cells (C-MSCs) are a novel mesenchymal stem cell (MSC) subpopulation derived from cardiac tissue, which are reported to be responsible for cardiac regeneration. Notch signaling is believed to aid in cardiac repair following myocardial injury. In this study, we have investigated the role of extracellular vesicles (EVs) from Notch1 engineered C-MSCs on angiogenesis and cardiomyocyte (CM) proliferation in ischemic myocardium.

miRNAs in Extracellular Vesicles from iPS-Derived Cardiac Progenitor Cells Effectively Reduce Fibrosis and Promote Angiogenesis in Infarcted Heart.

Cardiac stem cell therapy offers the potential to ameliorate postinfarction remodeling and development of heart failure but requires optimization of cell-based approaches. Cardiac progenitor cells (CPCs) induction by ISX-9, a small molecule possessing antioxidant, prosurvival, and regenerative properties, represents an attractive potential approach for cell-based cardiac regenerative therapy. Here, we report that extracellular vesicles (EV) secreted by ISX-9-induced CPCs (EV-CPC) faithfully recapitulate the beneficial effects of their parent CPCs with regard to postinfarction remodeling.

Fully automatic segmentation of 4D MRI for cardiac functional measurements.

Purpose: Segmentation of cardiac medical images, an important step in measuring cardiac function, is usually performed either manually or semiautomatically. Fully automatic segmentation of the left ventricle (LV), the right ventricle (RV) as well as the myocardium of three-dimensional (3D) magnetic resonance (MR) images throughout the entire cardiac cycle (four-dimensional, 4D), remains challenging. This study proposes a deformable-based segmentation methodology for efficiently segmenting 4D (3D + t) cardiac MR images.

Cardiac Progenitors Induced from Human Induced Pluripotent Stem Cells with Cardiogenic Small Molecule Effectively Regenerate Infarcted Hearts and Attenuate Fibrosis.

Cardiac progenitor cells (CPCs) being multipotent offer a promising source for cardiac repair due to their ability to proliferate and multiply into cardiac lineage cells. Here, we explored a novel strategy for human CPCs generation from human induced pluripotent stem cells (hiPSCs) using a cardiogenic small molecule, isoxazole (ISX-9) and their ability to grow in the scar tissue for functional improvement in the infarcted myocardium. CPCs were induced from hiPSCs with ISX-9.

Elevated circulating IL-32 presents a poor prognostic outcome in patients with heart failure after myocardial infarction.

Background: Interleukin-32 (IL-32) is a newly discovered proinflammatory cytokine. However, there are limited data regarding IL-32 as a biomarker for heart failure (HF). In this study, we assessed the prognostic value of IL-32 in patients with chronic HF after myocardial infarction (MI).

FGF23 promotes myocardial fibrosis in mice through activation of β-catenin.

Fibroblast growth factor 23 (FGF23) has been reported to induce left ventricular hypertrophy, but it remains unclear whether FGF23 plays a role in cardiac fibrosis. This study is attempted to investigate the role of FGF23 in post-infarct myocardial fibrosis in mice. We noted that myocardial and plasma FGF23 and FGF receptor 4 were increased in mice with heart failure as well as in cultured adult mouse cardiac fibroblasts (AMCFs) exposed to angiotensin II, phenylephrine, soluble fractalkine.

Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9.

Background: Transient preceding brief ischemia provides potent cardioprotection against subsequent long ischemia, termed ischemic preconditioning. Here, we hypothesized that transient short-term hypertrophic stimulation would induce the expression of hypertrophy regression genes and render the heart resistant to subsequent hypertrophic stress, and slow the progression to heart failure, as well.

Methods And Results: Cardiomyocyte hypertrophy was induced in mice by either transverse aortic constriction or an infusion of phenylephrine, and in neonatal rat ventricular cardiomyocytes by norepinephrine exposures.

Cytosolic CARP promotes angiotensin II- or pressure overload-induced cardiomyocyte hypertrophy through calcineurin accumulation.

The gene ankyrin repeat domain 1 (Ankrd1) is an enigmatic gene and may exert pleiotropic function dependent on its expression level, subcellular localization and even types of pathological stress, but it remains unclear how these factors influence the fate of cardiomyocytes. Here we attempted to investigate the role of CARP on cardiomyocyte hypertrophy. In neonatal rat ventricular cardiomyocytes (NRVCs), angiotensin II (Ang II) increased the expression of both calpain 1 and CARP, and also induced cytosolic translocation of CARP, which was abrogated by a calpain inhibitor.

Resveratrol improves myocardial ischemia and ischemic heart failure in mice by antagonizing the detrimental effects of fractalkine*.

Objectives: To test the hypothesis that resveratrol would improve cardiac remodeling by inhibiting the detrimental effects of fractalkine. We previously reported that fractalkine exacerbates heart failure. Furthermore, this study sought to determine whether resveratrol targets fractalkine to improve myocardial ischemia and cardiac remodeling.

Ultrasound molecular imaging of angiogenesis induced by mutant forms of hypoxia-inducible factor-1α.

Aims: Targeted point mutants of hypoxia-inducible factor-1α (HIF-1α) are potential optimal agents for angiogenesis therapy. Data are limited regarding the angiogenic response of HIF-1α mutants. We aimed to compare the angiogenic effect of wild-type and mutant HIF-1α by contrast ultrasound molecular imaging (UMI) of α(v)-integrin expression.

Detrimental effect of fractalkine on myocardial ischaemia and heart failure.

Aims: Fractalkine (FKN) is a newly identified membrane-bound chemokine; its role in myocardial ischaemia and heart failure is largely unknown. We attempted to investigate the role of FKN in myocardial ischaemia and ischaemia or pressure overload-induced ventricular remodelling and heart failure.

Methods And Results: FKN-induced changes of heart failure-related genes in cultured rat cardiac cells and the effect of FKN on cultured cardiomyocyte injury during anoxia/reoxygenation (A/R) were examined.

Deficiency of type 1 cannabinoid receptors worsens acute heart failure induced by pressure overload in mice.

Aims: We investigated the influence of type one cannabinoid receptor (CB1) deficiency on acute heart failure (AHF) and the underlying mechanism. Acute heart failure syndrome is an important clinical problem because of its high morbidity and mortality rates. Activation of CB1 induces vascular dilation and reinforces the properties of morphine, long-standing therapies for AHF syndrome, but the effect of endogenous CB1 activation on AHF is largely unknown.

Late-phase detection of recent myocardial ischaemia using ultrasound molecular imaging targeted to intercellular adhesion molecule-1.

Aims: in this study, we attempted to detect a recent myocardial ischaemic event using ultrasound molecular imaging (UMI) with microbubbles (MB) targeted to intercellular adhesion molecule-1 (ICAM-1) in the late phase of reperfusion.

Methods And Results: we created a myocardial ischaemia-reperfusion model in 60 C57/BL male mice to simulate an angina attack (ischaemia for 15 min, reperfusion for 1-24 h). The degree of myocardial inflammation and levels of ICAM-1 protein were determined by histological and immunohistochemical analyses.