Physiopathological Mechanisms Involved in the Progression of Pulmonary Fibrosis: A Systematic Review.

Q3 Medicine
Tanaffos Pub Date : 2022-03-01
Sana Bahri, Saloua Jameleddine
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引用次数: 0

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a lung disease characterized by formation of fibroblast foci and honeycomb lesions in the pulmonary parenchyma. The physiopathological mechanisms involved in the development of fibrosis and architectural disorganization are still imperfectly elucidated. In fact, lesion formation is irreversible and no treatment, to date, has been shown to be effective (30% of patients die within 5 years of the onset of the disease). The long-held concept of chronic inflammation leading to fibrosis is still controversial. Indeed, recent data suggest that the physiopathology of this disease is the product of fibroblast dysfunction rather than the result of an inflammatory imbalance. This concept supports the parallel involvement of three main factors: epithelial damage, angiogenesis and oxidative stress. In this review we highlighted the different factors and the ethiopathogenic pathways involved in the fibrotic process, in order to increase our understanding of the mechanisms involved in this pulmonary pathology.

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参与肺纤维化进展的生理病理机制:系统综述。
特发性肺纤维化(IPF)是一种肺部疾病,其特征是在肺实质中形成成纤维细胞灶和蜂窝状病变。参与纤维化和结构紊乱发展的生理病理机制仍未完全阐明。事实上,病变的形成是不可逆的,迄今为止没有任何治疗被证明是有效的(30%的患者在发病后5年内死亡)。长期以来,慢性炎症导致纤维化的概念仍然存在争议。事实上,最近的数据表明,这种疾病的生理病理是成纤维细胞功能障碍的产物,而不是炎症不平衡的结果。这一概念支持三个主要因素的平行参与:上皮损伤、血管生成和氧化应激。在这篇综述中,我们强调了纤维化过程中涉及的不同因素和埃塞俄比亚致病途径,以增加我们对这种肺部病理机制的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Tanaffos
Tanaffos Medicine-Critical Care and Intensive Care Medicine
CiteScore
1.10
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0.00%
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