Mechanistically distinct COX-2 inhibitors reduce stress-induced behavioral pathology via unique multimodal molecular mechanisms, and could be used to treat mood disorders.

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

A long non-coding RNA removes the transcriptional repressor p50 to regulate recruitment of co-activator p300 and RNA Polymerase II complexes to activate the COX-2 gene in human mammary epithelial cells and macrophages.

Local tissue hypoxia follows seizures, is responsible for postictal behavioural dysfunction rather than the seizures per se and can be treated.

PAK1 regulates inhibitory synaptic transmission in mice through a cyclooxygenase-2 dependent restriction in tonic, but not phasic, secretion of endocannabinoids.

During nephron regeneration, renal interstitial cells promote the proliferation of renal progenitor cells by secreting PGE2, thus forming the microenvironment of renal progenitor cells.

IL-33 plays an important role in the initiation of labor by leading to stress of the ER via an influx of calcium ions in human uterine smooth muscle cells.

Osteoblastic PGE2 induces pain and OA progression by Na_V1.8 modification and serves as a potential target multiple skeletal pain and degenerations.

CO₂/H⁺-dependent purinergic signaling by astrocytes provides specialized control of vascular tone in a brainstem respiratory center in a manner that contributes to respiratory behavior.

Salicylic acid, the precursor to aspirin, is an anti-tumor agent that blocks protein acetylation.