Results 121 to 130 of about 2,797,109 (304)

COPD advances in left ventricular diastolic dysfunction

open access: yes, 2016
Yoshiaki Kubota,1 Kuniya Asai,1 Koji Murai,1 Yayoi Tetsuou Tsukada,1 Hiroki Hayashi,2 Yoshinobu Saito,2 Arata Azuma,2 Akihiko Gemma,2 Wataru Shimizu1 1Department of Cardiovascular Medicine, 2Department of Pulmonary Medicine and Oncology, Graduate School
Gemma A   +8 more
core  

Irreversible left atrium dilatation preceding left ventricular dysfunction during trastuzumab therapy

open access: yes, 2018
Irreversible left atrium dilatation preceding left ventricular dysfunction during trastuzumab ...
Ribichini, Flavio   +7 more
core   +1 more source

Proteogenomic Profiling of Idiopathic Pulmonary Arterial Hypertension Identifies Sex‐Differential Proteins and Candidate Therapeutic Targets

open access: yesAdvanced Science, EarlyView.
An integrated proteogenomic analysis of 44,137 predominantly European‐ancestry UK Biobank participants aged 40–69 years identifies 12 robust proteins associated with idiopathic pulmonary arterial hypertension. These proteins define a high‐mortality molecular endotype, support early detection and mortality prediction, reveal sex‐differential proteomic ...
Xinjie Lin   +18 more
wiley   +1 more source

A novel porcine model of early left ventricular dysfunction for translational research

open access: yes, 2013
Nadim Malik, Kelly A Farrell, Sarah B Withers, Elizabeth J Wright, Cathy M HoltInstitute for Cardiovascular Science, University of Manchester, Manchester, United KingdomBackground: The early stages of left ventricular (LV) dysfunction account for a much ...
Farrell KA   +4 more
core  

Neuron‐Derived Vesicular circMagi1 Restrains Vascular Repair After Ischemic Stroke by Promoting TRIM65‐Mediated ANXA2 Degradation

open access: yesAdvanced Science, EarlyView.
After ischemic stroke, injured neurons transfer circMagi1 to endothelial cells through extracellular vesicles. Within endothelial cells, circMagi1 binds ANXA2 and enhances its engagement with TRIM65, promoting ANXA2 ubiquitination and proteasomal degradation to constrain angiogenic repair.
Youkun Bi   +16 more
wiley   +1 more source

A Hepatocyte‐to‐Stellate Cell Axis Couples Alternate‐Day Fasting to Liver Fibrosis Resolution via ATG7 S‐Nitrosylation

open access: yesAdvanced Science, EarlyView.
Alternate‐day fasting suppresses mitochondrial complex II assembly via SDHAF4 to upregulate hepatocyte eNOS. The resulting nitric oxide S‐nitrosylates ATG7 at C184 in hepatic stellate cells, restraining autophagic flux and preventing their profibrotic activation.
Xueqiang Wang   +17 more
wiley   +1 more source

Prognostic Value of Cardiac Troponin I and Left Ventricular Hypertrophy in Mortality of Chronic Hemodialysis Patients [PDF]

open access: yes
Cardiovascular events are the most common cause of death in hemodialysis patients. Cardiac biomarkers and especially Cardiac troponin I has been used as a prognostic marker in hemodialysis patients and there is some controversies about its value.
ذاکری, آناهیتا   +3 more
core  

Nuclear Translocation of PFKFB3 Promotes Disuse‐Induced Muscle Atrophy via Scaffolding Nedd4‐Mediated JunB Ubiquitination

open access: yesAdvanced Science, EarlyView.
Disuse‐induced muscle atrophy is driven by a non‐metabolic, nuclear function of the enzyme PFKFB3. Acting as a scaffold, PFKFB3 facilitates Nedd4‐mediated ubiquitination and degradation of the anti‐atrophy transcription factor JunB. Inhibiting this novel PFKFB3–Nedd4–JunB signaling axis stabilizes JunB and alleviates muscle wasting, revealing a highly ...
Mengjun Ma   +12 more
wiley   +1 more source

The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII‐δ

open access: yesAdvanced Science, EarlyView.
UCHL1 is highly upregulated in mice and patients with AF. UCHL1 directly binds to and removes K48‐linked polyubiquitin chains from CaMKII‐δ at K251 and enhances CaMKII‐δ stability, which activates RyR2, disrupts Ca2+ handling, and promotes AF. These findings establish UCHL1 as a critical regulator of CaMKII‐δ stability and AF‐related Ca2+ handling ...
Hai‐Lian Bi   +6 more
wiley   +1 more source

Salvianolic Acid a Disrupts the HSP90α‐AKT‐PERK Ternary Complex to Alleviate Atherosclerosis by Activating Endoplasmic Reticulum Stress of Senescent Vascular Smooth Muscle Cells

open access: yesAdvanced Science, EarlyView.
Salvianolic acid A (SAA) selectively induces senescent vascular smooth muscle cell apoptosis, alleviating atherosclerosis. Mechanistically, SAA targets heat shock protein 90 alpha (HSP90α) to disrupt the protein inase B (AKT)‐PRKR‐Like Endoplasmic Reticulum Kinase (PERK) scaffold, driving ubiquitin‐proteasome‐dependent AKT degradation.
Xiuya Guan   +8 more
wiley   +1 more source

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