New paradigms have been recently proposed in the pathogenesis of both chronic obstructive pulmonary disease\r\n(COPD) and idiopathic pulmonary fibrosis (IPF), evidencing surprising similarities between these deadly diseases,\r\ndespite their obvious clinical, radiological and pathologic differences. There is growing evidence supporting a\r\nââ?¬Å?double hitââ?¬Â pathogenic model where in both COPD and IPF the cumulative action of an accelerated senescence\r\nof pulmonary parenchyma (determined by either telomere dysfunction and/or a variety of genetic predisposing\r\nfactors), and the noxious activity of cigarette smoke-induced oxidative damage are able to severely compromise\r\nthe regenerative potential of two pulmonary precursor cell compartments (alveolar epithelial precursors in IPF,\r\nmesenchymal precursor cells in COPD/emphysema). The consequent divergent derangement of signalling\r\npathways involved in lung tissue renewal (mainly Wnt and Notch), can eventually lead to the distinct abnormal\r\ntissue remodelling and functional impairment that characterise the alveolar parenchyma in these diseases\r\n(irreversible fibrosis and bronchiolar honeycombing in IPF, emphysema and airway chronic inflammation in COPD).
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