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In another rodent experiment, synthetic TB4 was administered to models of autoimmune encephalomyelitis, markedly decreasing the number of inflammatory cells in the brains of the treated animals [39]

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Another study revealed a more specific mechanism underlying RV failure: under PAH conditions, circulating CCR2 + macrophages selectively infiltrate the RV and express high levels of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome, leading to mitochondrial dysfunction in cardiomyocytes