Results 231 to 240 of about 131,479 (353)

USP18 mediates high glucose‐induced cardiomyocyte injury by regulating the JAK/STAT signaling pathway through stabilizing FOXC2 expression

open access: yesJournal of Diabetes Investigation, EarlyView.
USP18 upregulation stabilizes FOXC2 expression by deubiquitination to inactivate the JAK2/STAT3 pathway, thereby inhibiting HG‐induced NMVM apoptosis, inflammation, oxidative stress, and fibrosis. ABSTRACT Background Cardiomyopathy is one of the complications of diabetes, among which myocardial fibrosis is the most typical feature.
Zhengrong Xu   +4 more
wiley   +1 more source

Combination of metformin and p38 MAPK inhibitor, SB203580, reduced myocardial ischemia/reperfusion injury in non‑obese type 2 diabetic Goto‑Kakizaki rats

open access: diamond, 2019
Jantira Sanit   +9 more
openalex   +2 more sources

Inhibition of dipeptidyl peptidase-IV enzyme activity protects against myocardial ischemia-reperfusion injury in rats [PDF]

open access: gold, 2014
Sarah Chua   +11 more
openalex   +1 more source

LIN28A blocks the EndMT process of high glucose‐induced HRMECs by stabilizing SIRT6 mRNA

open access: yesJournal of Diabetes Investigation, EarlyView.
LIN28A promotes mRNA stability of SIRT6 to activate the AMPK signaling, thereby inhibiting the EndMT process induced by HG in HRMECs. ABSTRACT Background Diabetic retinopathy (DR) is a microvascular condition resulting from microangiopathy, causing gradual retinal damage and potential blindness.
Xueying Wang   +5 more
wiley   +1 more source

Myocardial and Neural Damage due to Pulmonary Vein Isolation: Comparison of Pulsed Electric Field and Thermal Ablation

open access: yesPacing and Clinical Electrophysiology, EarlyView.
ABSTRACT Background Pulmonary vein isolation (PVI) using thermal energy—radiofrequency (RF) or cryoablation (CRYO)—is associated with direct myocardial injury and collateral neural damage. In contrast, pulsed electric field (PEF) energy has emerged as a neural‐sparing alternative.
Predrag Stojadinović   +12 more
wiley   +1 more source

The mitochondrial-derived peptide MOTS-c suppresses ferroptosis and alleviates acute lung injury induced by myocardial ischemia reperfusion via PPARγ signaling pathway

open access: hybrid, 2023
Peng Lü   +14 more
openalex   +1 more source

Exercise‐induced miR‐126 expression improves vascular health in prediabetes: A randomized controlled trial

open access: yesExperimental Physiology, EarlyView.
Abstract In this study, we investigated whether a structured aerobic exercise programme could enhance microRNA‐126 (miR‐126) expression and improve subclinical atherosclerosis markers [carotid intima–media thickness (CIMT) and ankle–brachial index (ABI)] in individuals with prediabetes.
Elif Yildirim Ayaz   +9 more
wiley   +1 more source

Senolytics and exercise: Dual modalities for rejuvenating muscle

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The role of senolytics on the heart and skeletal muscle. Senescent cell burden increases with ageing, disuse and disease. The senolytics dasatinib+quercetin (D+Q), navitoclax and fisetin, as well as exercise, eliminate senescent cells, reducing senescent cell burden and their senescence‐associated secretory phenotype (SASP ...
Zeynep Elif Yesilyurt‐Dirican   +4 more
wiley   +1 more source

Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia‐reperfusion injury

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Heart attack causes ischaemia–reperfusion injury in cardiomyocytes. Mitochondria generate reactive oxygen species (ROS), leading to oxidative stress. High levels of mitochondrial calcium (Ca2+) activate the mitochondrial permeability transition pore (mPTP), and excess ROS levels can lower the Ca2+ required to activate the mPTP ...
Emily Rozich   +5 more
wiley   +1 more source

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