Post‐COVID‐19 pulmonary fibrosis: Mechanisms, biomarkers, and therapeutic perspectives

Abstract

Abstract Post‐COVID‐19 pulmonary fibrosis (post‐CPF) has emerged as a serious complication with profound implications for long‐term respiratory health. This short review explores the multifactorial mechanisms underlying post‐CPF, emphasising the role of oxidative stress, epithelial‐to‐mesenchymal transition (EMT), and dysregulated immune responses. Key signalling pathways, such as TGF‐β, WNT, and Cadherin, are pivotal in fibrosis progression, offering potential therapeutic targets. Biomarkers, such as MUC4, KRT5, and ATP12A show promise for early detection and therapeutic targeting, as they share molecular features with idiopathic pulmonary fibrosis (IPF) and fibrotic interstitial lung diseases (f‐ILDs), suggesting opportunities to repurpose antifibrotic therapies. Despite these advancements, significant gaps remain in understanding the cellular and molecular mechanisms underlying fibrosis progression, hindering effective management of post‐CPF. Addressing these challenges through a targeted approach is critical to improving outcomes for survivors of severe COVID‐19.

Keywords

• diffuse alveolar damage
• fibrotic biomarkers
• immune dysregulation
• post‐COVID‐19 pulmonary fibrosis
• SARS‐CoV‐2