Results 191 to 200 of about 1,818,147 (330)
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
Impact of pulmonary infection and antibiotic use on recurrent myocardial infarction in patients with myocardial infarction. [PDF]
Liu Z+11 more
europepmc +1 more source
Experimental Myocardial Infarction in the Dog [PDF]
John Rees, V. J. Redding
openalex +1 more source
Bioprinted Organoids: An Innovative Engine in Biomedicine
Bioprinted organoids refer to either the printing of stem cells into tissue shape and subsequent differentiate into organoids, or assembling induced organoids as bioinks to replicate native organ. It enables the creation of miniaturized organs with complex architectures and physiological functions, potentially enhancing reproducibility, throughput, and
Zhengwei Li+11 more
wiley +1 more source
Implications of a new clinical classification of acute myocardial infarction. [PDF]
Thurston AJF+4 more
europepmc +1 more source
Glucose-Insulin-Potassium Therapy Guided by a Glucose-Controlled Insulin Infusion System in Acute Myocardinal Infarction [PDF]
Ball, P.+10 more
core +1 more source
Resection of Myocardial Aneurysms after Infarction during Temporary Cardiopulmonary Bypass [PDF]
C. Walton Lillehei+3 more
openalex +1 more source
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
Atrial Fibroblasts‐Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis
Exosome miR‐224‐5p derived from angiotensin II‐treated atrial fibroblasts creates a substrate for AF by promoting atrial electrical remodeling. Increased exosome miR‐224‐5p enhances AF susceptibility by inhibiting CACNA1c expression and decreasing ICa current of atrial cardiomyocytes.
Yue Yuan+13 more
wiley +1 more source