Results 191 to 200 of about 17,888 (258)

Redox Regulation and Oxidative Stress in Health and Disease: Mechanisms and Therapeutic Targeting

open access: yesMedComm – Future Medicine, Volume 5, Issue 2, June 2026.
Reactive species serve crucial roles which are tightly regulated in both physiological as well as disease states. At physiological levels, these species are integral to redox signaling, while uncontrolled redox promotes disease pathology. This review examines the dysregulation of these processes.
Mohammad Hossein Azadi   +2 more
wiley   +1 more source

Tubular Omega‐3 Fatty Acid Receptor FFAR4 Deficiency Aggravated Renal Aging and Chronic Kidney Disease

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
This study illustrates that omega‐3 PUFAs with their receptor FFAR4 alleviate tubular senescence and fibrosis in aged and fibrotic kidneys. Furthermore, we indicate that tubular FFAR4 improves renal senescence via 15d‐PGJ2‐PPARγ‐Klotho signaling, and suppresses kidney fibrosis by senescent tubular cell‐driven fibroblast activation.
Letian Yang   +9 more
wiley   +1 more source

Immunosenescence and Vaccine Efficacy in Aging: Dynamic Interplay of Gut Microbiota and mTOR Signaling Pathways

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
Aging impairs vaccine efficacy through gut microbiota dysbiosis and mTOR hyperactivation, which together drive inflammaging and weaken immune memory. This review highlights the bidirectional microbiota–mTOR axis and proposes that combining mTOR inhibitors with microbiota modulation offers a promising strategy to enhance vaccine responses in older ...
Jiaxuan Li   +5 more
wiley   +1 more source

Ligand‐Independent Activation of Notch1 by Cathepsin L Induces CUX1/p16INK4a‐Dependent Endothelial Senescence Associated With Atherosclerosis

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
CTSL activates Notch1/RBPJ in a ligand‐independent fashion, inducing CUX1/p16INK4a‐dependent endothelial senescence associated with atherosclerosis. ABSTRACT Our post‐GWAS functional analysis revealed that cathepsin L (CTSL) is an upstream regulator of CUX1, and it induces p16INK4a‐dependent and atherosclerosis‐associated senescence by indirectly ...
Yuwei Wu   +13 more
wiley   +1 more source

iLDA‐SGCN: Identifying Associations Between Age‐Related Diseases and Long Non‐Coding RNAs Using Dual Graph Convolutional Networks

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
iLDA‐SGCN integrates singular value decomposition and dual graph convolutional networks to predict lncRNA‐disease associations. It achieves superior performance on two benchmark datasets and identifies 33 candidate lncRNAs across 8 age‐related diseases.
Yu Guo   +8 more
wiley   +1 more source

Senescent BMSC‐Derived Thbs1 Drives Inflammaging and Impairs Bone Regeneration by Suppressing PINK1/Parkin‐Mediated Mitophagy in Macrophages

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
Aging BMSC‐derived Thbs1 activates the macrophage TGF‐β/Smad3 pathway to transcriptionally repress Pink1, impairing mitophagy and causing mitochondrial ROS accumulation. This redox imbalance drives M1 polarization and IL‐6 secretion. IL‐6 feeds back to BMSCs via the JAK/STAT3 pathway to inhibit osteogenesis and upregulate Thbs1, establishing a self ...
Yifeng Xing   +15 more
wiley   +1 more source

Lactobacillus paracasei L9 Ameliorates Pulmonary Fibrosis in Aged Mice via Gut‐Lung Axis‐Mediated Regulation of Immune Cell Migration

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
Oral administration of Lactobacillus paracasei L9 (L9) reshapes the gut microbiota, specifically increasing the abundance of short‐chain fatty acid (SCFA)‐producing bacteria (e.g., Blautia), thereby leading to a significant elevation of serum propionic acid (97% increase) and butyric acid (193% increase).
Ran Bi   +10 more
wiley   +1 more source

Cellular Senescence in Idiopathic Pulmonary Fibrosis: Molecular Mechanisms, Pathogenic Networks, and Emerging Therapeutic Targets. [PDF]

open access: yesDiseases
Baurzhan MB   +7 more
europepmc   +1 more source

Home - About - Disclaimer - Privacy