Results 141 to 150 of about 483,035 (267)
During renal fibrosis, SMAD3 acts as a transcription factor for CRLF1, promoting its expression and secretion. CRLF1 then binds to ITGB1 via an autocrine mechanism, activating the PI3K‐AKT signaling pathway to mediate renal fibrosis. This accelerates the progression from AKI to CKD, highlighting the therapeutic potential of targeting CRLF1 for ...
Chunjie Wang +8 more
wiley +1 more source
SDF‐1 levels decline significantly with maternal aging. Exogenous supplementation restores meiotic spindle morphology, chromosomal alignment, and mitochondrial function while reducing oxidative stress in aged oocytes. Mechanistically, SDF‐1 enhances autophagic activity to clear accumulated stress granules, thereby rescuing fertilization competence and ...
Rui Long +12 more
wiley +1 more source
Orphan GPCRs in diabetes mellitus: metabolic control, inflammation, and drug development. [PDF]
Chandrabose S +5 more
europepmc +1 more source
Astrocyte‐specific SHP1 deletion disrupts astrocyte–vascular interactions and compromises BBB integrity while enhancing STAT1‐dependent CXCL10 expression. These changes synergistically promote peripheral CD4+ and CD8+ T‐cell infiltration into the SDH. The infiltrating T cells secrete IFN‐γ, which in turn activates microglia.
Lan‐Xing Yi +7 more
wiley +1 more source
Antidiabetic medications and risk of cognitive disorders in type 2 diabetes: A retrospective cohort study. [PDF]
Nasir AB +11 more
europepmc +1 more source
VEGFR‐2 signaling in OSCC activates Src–STAT6‐dependent CSF2 transcription, driving tumor‐derived GM‐CSF secretion. GM‐CSF programs neutrophils to express PD‐L1 through STAT5–mTOR/S6K signaling, suppressing cytotoxic CD8+ T cells. This pathway reveals a tumor–neutrophil immune checkpoint circuit that limits anti‐PD‐1 responsiveness in OSCC.
Fangxing Zhu +13 more
wiley +1 more source
Pancreatic-liver crosstalk, novel molecular mediators, and 2025 therapeutic breakthroughs. [PDF]
Pan HY +9 more
europepmc +1 more source
A Novel Pak1 Activator Ameliorates ER Stress for HFpEF Therapy
Chronic metabolic stress is a major contributor to HFpEF progression. Under prolonged metabolic stress, Pak1 activity becomes impaired, contributing to disrupted ER proteostasis, cardiomyocyte apoptosis, fibrosis, and diastolic dysfunction. Mechanistically, Pak1 overexpression activates the ERK1/2–MNK1–eIF4E signaling axis, promotes translational ...
Honglin Xu +17 more
wiley +1 more source
Obesity-related Metabolic Dysfunction and Triple-negative Breast Cancer: Epidemiologic Signals, Mechanistic Pathways, and Opportunities for Prevention. [PDF]
Elkum N, Aboussekhra A.
europepmc +1 more source
High glucose is linked to reduced succinate dehydrogenase activity in CD14+ monocytes, accompanied by succinate accumulation and extracellular release. Extracellular succinate exacerbates mitochondrial ROS production and mtDNA release in CD4+ T cells. Cytosolic mtDNA then activates Z‐DNA binding protein 1 (ZBP1) and engages ZBP1‐associated inflammatory
Shuai Zhao +11 more
wiley +1 more source

