Results 141 to 150 of about 724,055 (291)

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

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

Lived experiences and perspectives of persons with conditions marked by autonomic dysfunction. [PDF]

open access: yesPLoS One
Shah LL   +17 more
europepmc   +1 more source

THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A

open access: yesAdvanced Science, EarlyView.
THSD7A exerts pro‐inflammatory effects and exacerbates atherosclerosis. Mechanistically, THSD7A regulates endothelial cell inflammation and atherosclerosis by activating the αvβ3/CEBPD/IL1A signaling axis. THSD7A is not only a genetic marker but also a potential therapeutic target for coronary artery disease (CAD).
Jiankun Liu   +15 more
wiley   +1 more source

The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies

open access: yesAdvanced Science, EarlyView.
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang   +5 more
wiley   +1 more source

Autonomic Dysfunction After Guillain-Barré Syndrome: Evidence from Comprehensive Autonomic Testing. [PDF]

open access: yesJ Clin Med
Theologou R   +7 more
europepmc   +1 more source

The Adipose‐Sympathetic Nerve Crosstalk: FSTL1 as an Adipocyte‐Derived Neurotrophic Factor for WAT Browning

open access: yesAdvanced Science, EarlyView.
As a novel adipose‐derived neurotrophic factor, Follistatin‐like 1 is endocytosed by sympathetic neurons primarily via tropomyosin‐related kinase B. This process promotes sympathetic innervation in adipose tissue and norepinephrine release, leading to white adipose tissue browning, enhanced thermogenesis, and anti‐obesity effects in mice.
Xiao‐Wei Jia   +13 more
wiley   +1 more source

Grtp1 Safeguards Against Paternal Reproductive Aging and Intergenerational Behavioral Deficits by Preserving Redox Homeostasis

open access: yesAdvanced Science, EarlyView.
This study identifies that Grtp1 maintains germline redox homeostasis by interacting with PRDX1/4‐TXN to antagonize paternal reproductive aging. Growth hormone restores Grtp1 expression, rectifies aberrant sperm DNA methylation, and ameliorates intergenerational anxiety and social deficits, highlighting the GH‐GRTP1 axis as a promising intervention ...
Yingdong Liu   +23 more
wiley   +1 more source

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