Review Article

Autophagy in Inflammatory Diseases

Figure 2

Autophagy as an adaptive cellular process potentially impacts the progression of inflammatory diseases by several possible mechanisms. (i) Autophagy, by acting as a “xenophagic” response, directly participates in bacterial clearance, through the encapsulation and lysosomal delivery of invading bacteria for degradation. (ii) Autophagic processes can assist in antigen presentation through the digestion of invading pathogens. (iii) Autophagic proteins play a role in the dampening proinflammatory responses, including proinflammatory cytokine secretion, through the maintenance of mitochondrial quality. (iv) Autophagic degradation of denatured protein aggregates may play a protective role in tissues such that impaired function has been associated with diseases such as cystic fibrosis [5]. (v) Autophagic protein LC3B potentially regulates other cellular processes as recently described in a model of hypoxia-induced pulmonary hypertension. In these studies, LC3B was found to inhibit vascular cell proliferation and promote smooth muscle cell apoptosis, collectively associated with protection in this model [29].
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