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Confocal microscopy (CM) and TEM demonstrate that classically activated pro-inflammatory macrophage (LPS + IFN--induced) actively orchestrate a distinct spatial uncoupling between the ER and mitochondria, thereby enforcing the glycolytic metabolic switch requisite for robust inflammatory effector functions

329,330 In degenerative joint diseases like OA, the metabolic balance of chondrocytes is disrupted, leading to the overproduction of degrading enzymes and inflammatory mediators, including iNOS, MMP-13, and ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5), which participate in cartilage degradation and inflammatory processes