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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders

Fig. 1

Pathways in pulmonary inflammation and potential therapeutic interventions. During pulmonary inflammation, proinflammatory factors like CSE, ATP, peptides (e.g., bradykinin, BK and endothelin-1, ET-1), cytokines (TNF-α and IL-1β), and endotoxins (e.g., LTA and LPS) increase. These factors induce inflammatory mediators (e.g., MMPs, adhesion molecules, COX-2, or cPLA2) through various signaling molecules, including mitochondrial or NOX-derived ROS generation, MAPKs activation, transactivation of growth factor receptors, and transcription factors in pulmonary resident cells (alveolar epithelial cells and tracheal smooth muscle cells). These changes lead to pathological alterations in these cells. Furthermore, potential therapeutic drugs such as PPAR agonists might protect against pulmonary inflammation by inducing antioxidant proteins like HO-1. It is hypothesized that these drugs induce HO-1 expression through ROS-dependent signals, directly preventing lung injury and inflammation

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Cell Communication and Signaling

ISSN: 1478-811X