Interaction of endoplasmic Reticulum stress responses to the vicinity of idiopathic pulmonary fibrosis: A potential target for a therapeutic approach

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by scar formation in the lung’s structure, progressive hypoxemia, dyspnea, body intolerance, and breathing difficulties. The diagnosis of IPF is difficult due to complex molecular mechanisms. In later stages, it will affect alveolar tissues, disrupt gaseous exchange, and ultimately lead to respiratory failure and death. The endoplasmic reticulum (ER) is essential for maintaining cellular homeostasis and protein secretions, lipid production, protein folding, and steroid synthesis or deposition. Numerous physiological and pharmacological conditions could affect ER homeostasis, which in turn influences the unfolded and misfolded protein responses that result in ER stress. The alveolar epithelium responds strongly to ER stress under IPF conditions, as evidenced by a biopsy of lung samples. Fibrotic disorders produce matrix-producing myofibroblasts. They have many wound-healing properties and may have distinct origins. The most often utilized marker is α-smooth muscle actin (SMA). However, the exact mechanism of ER stress in pulmonary fibrosis is still unknown. Therefore, in this review article, we have aimed to identify the disease-causing mechanism of IPF, understand the pathophysiology of alveolar cells during fibrotic response, and develop an effective drug to overcome this fibrotic disease. To develop logical strategies for modifying the senescent cell phenotype in the lung for therapeutic benefit, we have discussed the current understanding of the mechanism of IPF and the response of ER stress that regulates various aspects of cellular senescence related to chronic lung diseases.