Results 221 to 230 of about 7,324,613 (292)

Arylsulphatase A Pseudodeficiency (ARSA-PD), hypertension and chronic renal disease in Aboriginal Australians. [PDF]

open access: yesSci Rep, 2018
Tang D   +11 more
europepmc   +1 more source

OAF Blocks SIAH1‐Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD

open access: yesAdvanced Science, EarlyView.
This study shows OAF directly binds to SCPX and inhibits its interaction with the E3 ligase SIAH1, thereby protecting SCPX from ubiquitin‐dependent degradation and stabilizing its levels. This OAF‐SCPX axis represents a novel pathway in lipid homeostasis, highlighting OAF as a promising therapeutic candidate for MASLD.
Zongxi Li   +11 more
wiley   +1 more source

Natural Product Toosendanin Suppresses the Malignant Development of Skin Melanoma by Targeting BNC2 for Degradation

open access: yesAdvanced Science, EarlyView.
BNC2 exhibits context‐dependent opposing functions across multiple cancer types. This study reveals BNC2 as an oncogenic driver of melanoma proliferation and metastasis through transcriptional activation of PIK3CA. The natural compound TSN simultaneously degrades BNC2 and its oncogenic partner SMAD3 via CRBN‐dependent ubiquitination.
Hui Dai   +7 more
wiley   +1 more source

Evaluation of the effects of aerobic training during hemodialysis on autonomic heart rate modulation in patients with chronic renal disease. [PDF]

open access: yesMedicine (Baltimore), 2019
Morais MJD   +8 more
europepmc   +1 more source

14‐3‐3γ Protects Against Postoperative Cognitive Dysfunction by Regulating Tau Thr205 Phosphorylation and Synaptic Integrity

open access: yesAdvanced Science, EarlyView.
Integrative multi‐cohort analyses identify 14‐3‐3γ as a biomarker and regulator of cognitive vulnerability. Experimental studies show that 14‐3‐3γ loss is associated with Tau Thr205 phosphorylation, synaptic dysfunction, and cognitive impairment, while genetic overexpression or pharmacological stabilization of 14‐3‐3γ confers protective effects in ...
Shouqiang Zhu   +5 more
wiley   +1 more source

Reversing Macrophage Immunometabolic Dysfunction in Prolonged Infections Via a Glutaminolysis‐Fueled Restoration‐Based Hierarchically Selective Therapeutic System

open access: yesAdvanced Science, EarlyView.
A hierarchically selective immunotherapeutic nanoplatform, mGls@HEV‐MTP, selectively restores macrophage immunocompetence through GLS1‐mediated restoration of glutaminolysis‐fueled anaplerosis. Concurrently, it renders Staphylococcus aureus (S. aureus) more readily recognizable to the metabolically reprogrammed macrophages, thereby facilitating ...
Weinan Yang   +17 more
wiley   +1 more source

An Injectable ROS‐Responsive Nanozyme Hydrogel Regulates the Uterine Microenvironment to Prevent Intrauterine Adhesions

open access: yesAdvanced Science, EarlyView.
The injectable CeTA@GPP hydrogel is administered via intrauterine injection, forming a protective barrier. In the high ROS inflammatory microenvironment of injured endometrium, boronate ester cleavage triggers responsive CeTA release and local enrichment.
Peixian Cheng   +8 more
wiley   +1 more source

D4F‐Functionalized Ceria Nanozyme‐CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury

open access: yesAdvanced Science, EarlyView.
D4F‐functionalized ceria nanozyme–CasRx nanoparticles preferentially target renal macrophages through SR‐B1‐mediated uptake in ischemia–reperfusion injury. Ceria scavenges excessive ROS, while CasRx silences STING signaling, shifting macrophages toward a less inflammatory, pro‐resolving state and increasing the proportion of regulatory T cells.
Weibo Chen   +11 more
wiley   +1 more source

Interleukin‐1α Mediates Pancreatic Fibroblast Activation, Regulates Immune Cell Recruitment and Fibrosis in Acute and Chronic Pancreatitis

open access: yesAdvanced Science, EarlyView.
During pancreatitis, IL‐1α is released from necrotic acinar cells. In response to IL‐1α, pancreatic fibroblasts release chemokines and cytokines that regulate the recruitment of immune cells to the damaged organ. Furthermore, IL‐1α primes fibroblasts, resulting in increased tissue fibrosis during chronic pancreatitis.
Hala Mazloum   +13 more
wiley   +1 more source

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