Results 191 to 200 of about 338,002 (352)

Mitochondrial Transplantation Augments the Reparative Capacity of Macrophages Following Myocardial Injury

open access: yesAdvanced Science, EarlyView.
Mitochondrial transplantation induces macrophage polarization toward an anti‐inflammatory M2 phenotype, enhances their reparative capacities, and facilitates mitochondrial transfer to cardiomyocytes, collectively promoting tissue repair and functional recovery post‐myocardial infarction.
Yuning Zhang   +10 more
wiley   +1 more source

A Case of an Infected Right Ventricular Pseudo-False Aneurysm. [PDF]

open access: yesCureus
Hayashi Y   +4 more
europepmc   +1 more source

Ultrastructural Localization of Coxsackie B4 Virus in Mouse Myocardium [PDF]

open access: bronze, 1967
Rajindar S. Sohal   +3 more
openalex   +1 more source

PPP1R3B Suppresses Atherosclerosis by Promoting the M2 Polarization of Macrophages Through Glycogen Metabolic Reprogramming

open access: yesAdvanced Science, EarlyView.
PPP1R3B induces anti‐inflammatory M2 macrophage polarization and maintains energy supply in plaques. Its absence accelerates plaque progression. PPP1R3B regulates M2 macrophage polarization and energy metabolism via phosphorylated STAT3 (p‐STAT3), which plays a dual role by activating anti‐inflammatory transcriptional programs through the PPAR‐γ/PGC‐1α/
Lin Shen   +12 more
wiley   +1 more source

Surgical lead extraction for pacemaker infection with tricuspid valve repair: A case report. [PDF]

open access: yesSAGE Open Med Case Rep
Hisata Y   +5 more
europepmc   +1 more source

FMO2 Promotes Angiogenesis via Regulation of N‐Acetylornithine

open access: yesAdvanced Science, EarlyView.
This study identifies flavin‐containing monooxygenase 2 (FMO2) as a novel proangiogenic regulator in endothelial cells. Targeted FMO2 ablation impairs vessel sprouting, whereas its compensation potently enhances angiogenesis. Metabolomics and single‐cell sequencing reveal that FMO2 drives vascular growth via the N‐acetylornithine/ATF3/NOTCH1 axis ...
Jingyi Wang   +15 more
wiley   +1 more source

PM2.5 Induce Endothelial‐Mesenchymal Transition and Cardiac Fibrosis via the NCOA4‐Mediated Ferritinophagy

open access: yesAdvanced Science, EarlyView.
This study primarily reveals that PM2.5‐derived Fe‐containing particles, particularly magnetite, are specifically enriched in the heart. Here, they interact with NCOA4 in endothelial cells, disrupt iron homeostasis by enhancing ferritinophagy, and subsequently trigger the process of EndMT through the NCOA4/KLF5 pathway.
Qinglin Sun   +11 more
wiley   +1 more source

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