Results 191 to 200 of about 96,194 (242)

Astrocytic Phenotypic Switching in Posterior Piriform Cortex Orchestrates Bone Cancer Pain–Depression Comorbidity via Purinergic–Noradrenergic Signaling

Advanced Science, EarlyView.
Bone cancer pain and depression share a common origin: astrocytic A2‐to‐A1 transition in the posterior piriform cortex. This phenotypic shift disrupts the ATP–adenosine–A2AR–norepinephrine axis, simultaneously driving nociceptive and affective dysfunction.
Jiang‐Ping Liu, Jun‐Han Zhang, Zhi‐Xuan Tan, Wei‐Bing Yan, Ya‐Ru Yuan, Yao Liu, Bing‐Di Wei, Meng‐Qi Ding, Zhuo‐Min Fu, Ying Liu, An‐Qi Wang, Lin Ma, Yong‐Hong Li, Er‐Qing Chai, Chao‐Jun Wei   +14 more
wiley   +1 more source

Quantitative systems pharmacology model of α-synuclein pathology in Parkinson's disease-like mouse for investigation of passive immunotherapy mechanisms. [PDF]

CPT Pharmacometrics Syst Pharmacol
Ivanova O, Karelina T.
europepmc   +1 more source

VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain

Advanced Science, EarlyView.
The mechanism diagram of VDAC1 mediating neuronal excitability and neuropathic pain. Briefly, VDAC1 is expressed in DRG neurons and is upregulated following CCI‐induced neuropathic pain. This upregulation enhances ATP transport from mitochondria to the cytoplasm in sensory neurons, leading to increased neuronal excitability and pain behavior.
Fengrun Sun, Ning Yu, Liang Yu, Xiaofen Tian, Yujia Ma, Yikuan Xie, Tao Wang, Chao Ma   +7 more
wiley   +1 more source

Optimizing Clinical Translation of Bispecific T-cell Engagers through Context Unification with a Quantitative Systems Pharmacology Model. [PDF]

Clin Pharmacol Ther
Liao X, Qi T, Zhou J, Liu C, Cao Y.
europepmc   +1 more source

TOLLIP Inhibits Psoriasis Progression via Suppressing PKM2‐Mediated Glycolysis in Keratinocytes

Advanced Science, EarlyView.
In this study, we identify TOLLIP as a critical regulator of psoriasis pathogenesis through its modulation of glycolytic metabolism. Our findings establish the TOLLIP‐PKM2‐glycolysis axis as a key mechanism linking metabolic reprogramming to psoriasis pathogenesis, and propose TOLLIP as a promising therapeutic target.
Xiuhuan Jiang, Guoying Miao, Na Shen, Qingxia Han, Xiaoru Han, Zichang Qiao, Kexin Feng, Zhuo Tan, Yaguang Wang, Xiuhua Liu, Chen Wu, Zhenzhen Yan   +11 more
wiley   +1 more source

Creating a Roadmap to Quantitative Systems Pharmacology-Informed Rare Disease Drug Development: A Workshop Report. [PDF]

Clin Pharmacol Ther
Bai JPF, Stinchcomb AL, Wang J, Earp J, Stern S, Schuck RN.   +5 more
europepmc   +1 more source

Loss of E3 Ubiquitin Ligase RINES via CpG Methylation Relieves Suppression of STAT3 and MYC, Facilitating Multiple Tumorigeneses

Advanced Science, EarlyView.
Dysregulated protein modifications drive tumorigenesis. RINES, an E3 ubiquitin ligase, represses tumor cell proliferation and metastasis by facilitating RING domain‐dependent, ubiquitin–proteasome‐mediated degradation of STAT3 and MYC, which consequently restrains cancer stemness and oncogenic progression.
Lili Li, Ka Man Ng, Xingsheng Shu, Xiaoxue Chai, Kai Yau Wong, Gopesh Srivastava, Anthony T.C. Chan, Wai Yee Chan, Qian Tao   +8 more
wiley   +1 more source

Quantitative systems pharmacology modeling of tumor heterogeneity in response to BH3-mimetics using virtual tumors calibrated with cell viability assays. [PDF]

CPT Pharmacometrics Syst Pharmacol
Derippe T, Fouliard S, Decleves X, Mager DE.   +3 more
europepmc   +1 more source

BIN1 and ALDH1B1 Deficiency in Colonic Smooth Muscle Drives Mitochondrial Dysfunction and Fibrosis in Slow‐Transit Constipation

Advanced Science, EarlyView.
Slow‐transit constipation (STC) is a disabling motility disorder with unclear smooth‐muscle mechanisms. Spatial proteomic analysis of STC patient colon reveals both the central pathogenic role of smooth muscle cells (SMCs) in STC and novel regulators of intestinal motility, BIN1 and ALDH1B1.
Jianbo Liu, Hao Zhang, Wenhao Qiao, Ran Liu, Jie Sun, Xiaopei Li, Qin Li, Dongbo Zhao, Dawei Chen, Jingxin Li, Shuxiao Dong   +10 more
wiley   +1 more source