Results 81 to 90 of about 39,202 (243)
In PWS‐ASPCs, FOSL1 drives the expression of SPSB1. SPSB1, as part of the ESC complex, further binds to HDAC1 and promotes K29‐linked and K48‐linked polyubiquitination of HDAC1. These modifications facilitate the degradation of HDAC1 through the ALP and UPS pathways, respectively.
Hongrui Chen +5 more
wiley +1 more source
Human dental pulp stem cell secretome emerges as a cell‐free therapeutic strategy for ischemic stroke by reprogramming redox and inflammatory signaling. hDPSC secretome‐derived antioxidant and immunomodulatory factors suppress the TLR4–NOX–ROS–NF‐κB axis, reduce microglial inflammatory responses and apoptosis, and promote neurogenesis, angiogenesis ...
Kyung‐Joo Seong +8 more
wiley +1 more source
This study identifies that the PD‐associated TMEM175‐L156P variant disrupts lysosomal ion channel trafficking by causing aberrant endoplasmic reticulum retention. A “chaperone–agonist” bifunctional small molecule restores TMEM175‐L156P lysosomal localization and channel function, thereby alleviating PD‐relevant cellular phenotypes and highlighting a ...
Ting Luo +17 more
wiley +1 more source
In diabetic kidney disease, elevated podocyte ANGPTL4 is linked to reduced TFEB nuclear localization and compromised lysosomal degradative function. These changes impair podocyte lipophagy and promote lipid‐droplet accumulation and podocyte injury, which may contribute to renal injury progression.
Xiaojing Liu +7 more
wiley +1 more source
Systemic platelet factor 4 (PF4) is significantly depleted in amyotrophic lateral sclerosis (ALS). Peripheral PF4 replenishment restores central proteostasis by driving OPTN‐dependent, PINK1‐independent selective autophagy in motor neurons. This intervention effectively clears toxic SOD1 aggregates, blunts glial activation, and preserves neuromuscular ...
Qingjian Xie +12 more
wiley +1 more source
The endoplasmic reticulum, not the pH gradient, drives calcium refilling of lysosomes
Impaired homeostasis of lysosomal Ca2+ causes lysosome dysfunction and lysosomal storage diseases (LSDs), but the mechanisms by which lysosomes acquire and refill Ca2+ are not known.
Abigail G Garrity +5 more
doaj +1 more source
A cationic poly(disulfide)‐drug nanoplatform (LA/DexP) was developed to treat experimental autoimmune uveitis (EAU). With potent blood‐retinal barrier penetrability, LA/DexP releases DSP in response to high ROS and scavenges cfDNA to inhibit the cGAS‐STING signaling pathway.
Yuelan Wu +12 more
wiley +1 more source
Resolution pharmacology is an emerging strategy to tackle inflammatory pathologies. Bioinspired meroterpenoids induce a lipid mediator class switch toward inflammation resolution in vitro and in vivo by targeting key nodes in lipid mediator biosynthesis and neutral lipid dynamics.
Lorenz Waltl +20 more
wiley +1 more source
USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis
This study reveals that USP5 drives vascular smooth muscle cell senescence and atherosclerosis by stabilizing TGFBR1, suppressing IDH2, and promoting glycolytic reprogramming, identifying the USP5‐TGFBR1‐IDH2 axis as a potential therapeutic target. ABSTRACT Vascular smooth muscle cell (VSMC) senescence contributes importantly to atherosclerotic plaque ...
Xinhai Cui +5 more
wiley +1 more source
Lysosomal diseases: Overview on current diagnosis and treatment
Lysosomal diseases (LDs), also known as lysosomal storage diseases (LSDs), are a heterogeneous group of conditions caused by defects in lysosomal function.
Fabiano de Oliveira Poswar +8 more
doaj +1 more source

