Pulmonary fibrosis is a highly heterogeneous and lethal condition with limited therapeutic options. Recent studies have identified new pathogenic mechanisms involved in the initiation and progression of fibrosis. A detailed understanding of the cellular and molecular mechanisms underlying pulmonary fibrosis could pave the way for effective therapeutics. Inflammation plays a crucial role in the progression of some forms of pulmonary fibrosis, with proinflammatory mediators such as TNF, IL-1β, and IL-17A contributing to the disease. The involvement of Th2 responses and IL-13 in fibrosis is also highlighted, along with the role of chemokines in recruiting leukocytes and fibroblasts to the lung. Additionally, factors influencing epithelial cell and fibroblast differentiation and proliferation, such as the Wnt-β-catenin signaling pathway and epigenetic changes, are discussed. The review also explores potential therapeutic targets, including PPARs and microRNAs, and the disease stage-specific roles of macrophages. Overall, a more integrated approach targeting multiple aspects of the fibrotic process is needed to develop effective treatments for this complex and devastating disease.Pulmonary fibrosis is a highly heterogeneous and lethal condition with limited therapeutic options. Recent studies have identified new pathogenic mechanisms involved in the initiation and progression of fibrosis. A detailed understanding of the cellular and molecular mechanisms underlying pulmonary fibrosis could pave the way for effective therapeutics. Inflammation plays a crucial role in the progression of some forms of pulmonary fibrosis, with proinflammatory mediators such as TNF, IL-1β, and IL-17A contributing to the disease. The involvement of Th2 responses and IL-13 in fibrosis is also highlighted, along with the role of chemokines in recruiting leukocytes and fibroblasts to the lung. Additionally, factors influencing epithelial cell and fibroblast differentiation and proliferation, such as the Wnt-β-catenin signaling pathway and epigenetic changes, are discussed. The review also explores potential therapeutic targets, including PPARs and microRNAs, and the disease stage-specific roles of macrophages. Overall, a more integrated approach targeting multiple aspects of the fibrotic process is needed to develop effective treatments for this complex and devastating disease.