Post-Covid-19 Pulmonary Fibrosis: Pathogenesis, Risk Factors, Diagnosis, And Emerging Therapeutic Strategies

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to significant global morbidity and mortality. While many patients recover, a subset experiences persistent pulmonary complications, including post-COVID-19 pulmonary fibrosis (PCPF), a condition characterized by irreversible lung scarring and impaired gas exchange. Several risk factors, such as advanced age, male sex, pre-existing lung disease, and severe COVID-19 requiring mechanical ventilation, contribute to its development. Radiological assessments, particularly high-resolution computed tomography, reveal hallmark features such as reticular opacities, traction bronchiectasis, and parenchymal bands, aiding in diagnosis. Current therapeutic strategies include corticosteroids, antifibrotic agents (pirfenidone, Nintedanib), and immunosuppressants, though no standardized treatment exists. Pulmonary rehabilitation and supplemental oxygen therapy offer symptomatic relief and improved functional outcomes. Future research explores novel agents, including buloxibutid, saracatinib, sirolimus, and resveratrol, as potential antifibrotic therapies. This review provides an overview of the pathogenesis, clinical manifestations, diagnostic approaches, and evolving treatment strategies for PCPF, emphasizing the need for continued research to optimize patient outcomes. Key words: SARS-CoV-2, ARDS, Pulmonary Fibrosis, fibroblasts, Pirfenidone, Nintedanib