Results 121 to 130 of about 5,850,068 (304)
The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII‐δ
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
Trained immunity and atherosclerotic cardiovascular disease
Purpose of review The two major challenges in cardiovascular medicine are to refine risk prediction and to improve pharmacological prevention and treatment. The concept of innate immune memory, which is called trained immunity, has the potential to improve clinical practice in these regards ...
openaire +4 more sources
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
Introduction Previous studies have linked placental weight (PW) to cardiovascular diseases, but the causality and potential mediators underlying this relationship are still unknown. Material and methods We conducted Mendelian randomization (MR) analysis
Shilin Fan +7 more
core +1 more source
Efficacy and safety of drugs in residual cardiovascular risk: A systematic review of the literature
Background: The objective of this research is to evaluate the efficacy and safety of drugs in the residual risk in any of its three components: lipid, inflammatory and thrombotic risk.
Mario Andres Hernandez-Sómerson +2 more
doaj +1 more source
CD72hi macrophages drive endothelial pyroptosis and accelerate atherosclerosis through CXCL12–CXCR4‐mediated immune–vascular crosstalk. Ilexoside K suppresses this pathogenic communication by modulating CXCR4‐dependent endothelial responses, reducing inflammation and plaque progression. These findings reveal a macrophage–endothelial regulatory axis and
Xingling He +11 more
wiley +1 more source
The mechanobiological basis of atherosclerotic progression and its contribution to spatial and temporal heterogeneity remain incompletely understood. Spatially resolved AFM measurements revealed that plaque formation and distinct regions (cap fibrosis, intimal fibrosis, and lipid‐rich core) exhibit heterogeneous elastic modulus and viscoelastic ...
Yidan Zhou +13 more
wiley +1 more source
Regulatory mechanisms of monocytes and macrophages in atherosclerotic cardiovascular disease [PDF]
Atherosclerotic cardiovascular disease is a leading cause of mortality. Given the importance of monocytes and macrophages in all stages of atherosclerotic development and progression, understanding their regulatory mechanisms can inform the development ...
Kempkes, R.W.M.
core +2 more sources
Cigarette tar triggers EC‐derived EVs carrying TDP43, which binds VDAC1 to boost MAMs, mitochondrial Ca2+ overload, and METs formation in macrophages, accelerating smoking‐related AS progression, while retinoic acid binds TDP43 to block this pathogenic cascade.
Xinxin Zhu +20 more
wiley +1 more source
Under pathological stimulation, NCOA4 in macrophages interacts with STAT1 to promote CH25H transcription. The subsequent increase in 25‐HC production activates macrophages, triggers inflammatory responses and ferroptosis, and accelerates the progression of AAA.
Zhinan Wu +9 more
wiley +1 more source

