Results 121 to 130 of about 8,670,383 (247)

KLF5 Downregulation Links Impaired BNIP3‐Mediated Mitophagy to Inflammatory Valve Remodeling in Calcific Aortic Valve Disease

open access: yesAdvanced Science, EarlyView.
In human CAVD, KLF5 is reduced in VIC‐rich regions and remodeling/stress‐associated VIC states. In VICs, KLF5 sustains BNIP3 promoter activity and BNIP3‐mediated mitophagy, thereby limiting cytosolic mtDNA accumulation. KLF5 loss weakens mitochondrial quality control and enhances mtDNA‐sensitive STING/NF‐κB/NLRP3 inflammatory signaling under osteogenic
Jin‐Hui Bian   +13 more
wiley   +1 more source

SerpinA3 is an Endogenous TGF‐β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling

open access: yesAdvanced Science, EarlyView.
SerpinA3 acts as an endogenous TGF‐β receptor antagonist that binds to the extracellular domain of TGFR‐1, thereby preventing TGFR‐1–TGFR‐2 complex formation. This receptor‐level blockade suppresses TGF‐β/Smad2/3 signaling, attenuates cardiac fibroblast activation, and extracellular matrix deposition, and ultimately alleviates pressure overload–induced
Hui Wang   +9 more
wiley   +1 more source

Dual pKa Lipid Nanoparticles for Lung‐tropic mRNA Delivery and pH‐Programmed Endosomal Escape

open access: yesAdvanced Science, EarlyView.
Lipid nanoparticles’ bottleneck lies in low endosomal escape efficiency and liver‐dominant delivery after intravenous administration. To overcome these limitations, we present a stepwise pH‐programmed lipid nanoparticle system enabled by our newly synthesized ionizable lipid.
Seong Gi Lim   +12 more
wiley   +1 more source

The brain in heart failure [PDF]

open access: yes, 2004
After atrial fibrillation, heart failure is the second most frequent cardiac association of stroke. Deteriorating left ventricular systolic function appears to increase the risk of cardioembolic stroke in heart failure.
Pullicino, Patrick
core   +1 more source

Macrophage PARP7 Alleviates Septic Cardiomyopathy by Interacting With TBK1 and Suppressing TBK1‐Driven Inflammatory Response

open access: yesAdvanced Science, EarlyView.
In septic cardiomyopathy, PARP7 directly binds TBK1 and mediates its ADP‐ribosylation, thereby repressing TBK1‐driven proinflammatory signaling in macrophages. ABSTRACT Septic cardiomyopathy is a life‐threatening complication of sepsis, and an uncontrolled inflammatory response represents a key pathogenic mechanism. PARP7 negatively regulates the IFN‐I
Jibo Han   +10 more
wiley   +1 more source

Physiological and clinical consequences of relief of right ventricular outflow tract obstruction late after repair of congenital heart defects. [PDF]

open access: yes, 2006
BACKGROUND: Right ventricular outflow tract obstruction (RVOTO) is a common problem after repair of congenital heart disease. Percutaneous pulmonary valve implantation (PPVI) can treat this condition without consequent pulmonary regurgitation or ...
Sridharan, S   +10 more
core  

Niche‐Mediated Neural Priming Enables Robust and Scalable Generation of Human Choroid Plexus Organoids

open access: yesAdvanced Science, EarlyView.
Compared to E8, mTeSR1 culture downregulated WNT and TGF‑β signaling, and upregulated neural differentiation pathways, enhancing neural priming. Under skin organoid induction conditions, mTeSR1‑cultured hESCs generated organoids with significantly higher neuroepithelial differentiation.
Zhongliang Chen   +7 more
wiley   +1 more source

Nrsn1–Smarcc1 Coupling Regulates Neural Stem Cell Differentiation and Chronic‐phase Recovery After Ischemic Stroke

open access: yesAdvanced Science, EarlyView.
In the post‐stroke brain, Foxa2 induces the transcriptional upregulation of Nrsn1 in NSCs. Nrsn1 functionally couples with Smarcc1, modulating its nuclear availability and protein abundance, thereby influencing Smarcc1‐associated regulatory programs linked to neuronal lineage commitment. Through this coupling, Nrsn1 promotes the differentiation of NSCs
Ruolin Zhang   +18 more
wiley   +1 more source

Mitochondria‐Targeted Multimodal Nanotherapeutics Suppress Oxidized mtDNA‐Driven Inflammation at the Source

open access: yesAdvanced Science, EarlyView.
Ox‐mtDNA fragments escaping from mitochondria drive robust inflammatory responses. A targeted nanoplatform simultaneously inhibits mitochondrial FEN1‐mediated mtDNA cleavage and scavenges ROS, preventing the generation of immunogenic Ox‐mtDNA fragments. The released SeNPs further promote autophagic clearance of cytosolic mtDNA. Consequently, cGAS‐STING,
Wen‐Ling Li   +7 more
wiley   +1 more source

Moexipril and left ventricular hypertrophy

open access: yes, 2007
George S Chrysant1, PK NguyenUniversity of Oklahoma, 1Director, Advanced Cardiac Imaging, INTEGRIS Heart Hospital, Oklahoma City, OK, USAAbstract: Angiotensin-converting enzyme (ACE) inhibitors today are the standard therapy of patients with myocardial ...
George S Chrysant, PK Nguyen
core  

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