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Anti-inflammatory effects of resveratrol are mediated by the estrogen receptor to coordinate a complex array of transcriptional coregulators, suggesting that estrogenic effects must be considered in the complex polypharmacology of resveratrol.

Glutamine deprivation reprograms chondrocytes, attenuates inflammation, and such intervention may be protective against joint inflammation.

Intercellular interactions between fibrocytes and CD8⁺ T lymphocytes promote inflammation through a pathophysiological positive feedback loop in bronchi of patients with chronic obstructive pulmonary disease (COPD).

Gαq stimulates HDAC5 phosphorylation by PKC-independent PKD/PKCμ activation to induce the IκB expression and limit the NF-κB-mediated inflammatory response which essential for proper endometrial decidualization and early pregnancy.

Inflammatory dynamics are tailored to bacterial class through macrophage integration of microbial stimuli and cytokine feedback.

Distinct hematopoietic waves interact via transcriptional cascades specific to embryonic hemocytes to ensure the proper immune response in Drosophila.​.

Oligodendrocytes with an enhanced ability to withstand cytotoxic stress display an increased capacity to remyelinate demyelination lesions of the CNS in the presence of an inflammatory environment.

Thermal injury and infected wounds induce distinct inflammatory and remodeling mechanisms that alter the dynamics of wound repair.

RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.

Tyrosine phosphorylation of the intracellular domain of LRP1 serves as a molecular switch to regulate cellular cholesterol homeostasis through nuclear hormone receptor-mediated regulation of the cellular cholesterol exporter ABCA1.