Results 161 to 170 of about 321,368 (335)

ALKBH5‐Mediated M6A Demethylation of G3BP1 Attenuates Ferroptosis Via Cytoplasmic Retention of YBX1/p53 in Diabetic Myocardial Ischemia‐Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
ALKBH5 promoted G3BP1 expression via m⁶A methylation at sites 142/173. G3BP1 interacts with YBX1 and p53, reducing their nuclear translocation and decreasing p53‐mediated SLC7A11 repression. This inhibites cardiomyocyte ferroptosis and mitigates myocardial damage during diabetic ischemia‐reperfusion injury.
Wenyuan Li   +5 more
wiley   +1 more source

Role of pathogen-laden expiratory droplet dispersion and natural ventilation explaining a COVID-19 outbreak in a coach bus. [PDF]

open access: yesBuild Environ, 2022
Luo Q   +8 more
europepmc   +1 more source

LncRNA Foxo6os as a Novel “ Scaffold” Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure

open access: yesAdvanced Science, EarlyView.
Schematic overview showing that forkhead box O6, opposite strand (Foxo6os) acts as a “scaffold”, directly binding myosin‐binding protein‐C (MYBPC3) and recruiting protein kinase C (PKC‐α) to mediate site‐specific phosphorylation of MYBPC3. This post‐translational modification supports cardiac contraction by regulating L‐type Ca2+ channels, especially ...
Jie Sheng   +9 more
wiley   +1 more source

Succinic Acid‐Induced Macrophage Endocytosis Promotes Extracellular Vesicle‐Based Integrin Beta1 Transfer Accelerating Fibroblast Activation and Sepsis‐Associated Pulmonary Fibrosis

open access: yesAdvanced Science, EarlyView.
Lipopolysaccharide (LPS) stimulates the production of succinic acid in lung tissue, which promotes macrophages endocytosis and the formation of multivesicular bodies (MVBs). These MVBs release profibrotic extracellular vesicles (EVs), facilitating the transfer of integrin beta1 (ITGβ1) transfer and subsequently activating fibroblasts, thereby ...
Wenyu Yang   +10 more
wiley   +1 more source

FOXM1 Protects Against Myocardial Ischemia‐Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1‐Dependent LKB1 Ubiquitination

open access: yesAdvanced Science, EarlyView.
FOXM1 maintains mitochondrial bioenergetic function by inhibiting MKRN1‐mediated ubiquitination of LKB1 in cardiomyocytes. Loss of FOXM1 in cardiomyocytes results in upregulation of MKRN1, which enhances LKB1 ubiquitination and disrupts AMPK signaling and energy metabolism pathways. Conversely, FOXM1 overexpression preserves mitochondrial bioenergetics
Shuai Song   +17 more
wiley   +1 more source

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