Department of Biological Sciences, NIPER Hyderabad, Balanagar, Hyderabad, India.
Department of Biology, University of Saskatchewan, Saskatoon, SK S7N 5E2, Canada.
Int Immunopharmacol. 2023 Mar;116:109418. doi: 10.1016/j.intimp.2022.109418. Epub 2022 Nov 4.
COVID 19, a lethal viral outbreak that devastated lives and the economy across the globe witnessed non-compensable respiratory illnesses in patients. As been evaluated in reports, patients receiving long-term treatment are more prone to acquire Pulmonary Fibrosis (PF). Repetitive damage and repair of alveolar tissues increase oxidative stress, inflammation and elevated production of fibrotic proteins ultimately disrupting normal lung physiology skewing the balance towards the fibrotic milieu.
In the present work, we have discussed several important pathways which are involved in post-COVID PF. Further, we have also highlighted the rationale for the use of antifibrotic agents for post-COVID PF to decrease the burden and improve pulmonary functions in COVID-19 patients.
Based on the available literature and recent incidences, it is crucial to monitor COVID-19 patients over a period of time to rule out the possibility of residual effects. There is a need for concrete evidence to deeply understand the mechanisms responsible for PF in COVID-19 patients.
COVID-19 是一场致命的病毒性疫情，在全球范围内给人们的生命和经济带来了毁灭性的影响，并导致患者出现不可补偿的呼吸系统疾病。据报道，接受长期治疗的患者更容易患上肺纤维化（PF）。肺泡组织的反复损伤和修复会增加氧化应激、炎症和纤维化蛋白的产生，最终破坏正常的肺生理功能，使纤维化环境失衡。
在目前的工作中，我们讨论了几个涉及 COVID 后 PF 的重要途径。此外，我们还强调了使用抗纤维化药物治疗 COVID 后 PF 的合理性，以减轻 COVID-19 患者的负担并改善其肺功能。
根据现有文献和最近的发病情况，有必要在一段时间内对 COVID-19 患者进行监测，以排除残留效应的可能性。需要具体的证据来深入了解 COVID-19 患者发生 PF 的机制。
