Abstract
Pulmonary fibrosis is a disease of the lower respiratory system. It might be as Idiopathic fibrosis which is obscure reason for disease or might be as an optional impact from different causes, for example, the environmental causes, for example, toxins and smoking, some connective tissue illnesses., infection diseases, for example, tuberculosis (TB) and corona virus, a few medications, for example, bleomycin, methotrexate, and radiation treatment. Glucocorticoid are used for treating inflammatory and immune diseases, like asthma, but interstitial lung disease, cystic fibrosis, and chronic obstructive pulmonary disease (COPD) at some stage, may become resistant to corticosteroid treatment. Glucocorticoids inhibit inflammation by many mechanisms. The oxidative stress leads to significantly decrease in activity and expression of Histone deacetylase 2 (HDAC-2) which causes resistant to the action of glucocorticoid. However, the dissociated glucocorticoids have been developed to decrease side effects, the dissociated glucocorticoid receptor agonists (DIGRAs) are a class of experimental drugs designed to share many of the desirable anti-inflammatory, immunosuppressive, or anticancer properties of classical glucocorticoid drugs with fewer side effects, but it is so difficult to dissociate anti-inflammatory effects from adverse effects. Patients with glucocorticoid resistance must use alternative anti-inflammatory treatments as well as drugs that may reverse the molecular mechanism of glucocorticoid resistant. Objective: This paper is to review the corticosteroid resistant pulmonary fibrosis and how overcome this resistance.
 The data was collected from December 2020 to September 2021.
Highlights
The interstitial lung diseases (ILDs) are different classification of lung diseases that are characterized by prolonged inflammation and progressive fibrosis of the pulmonary interstitium [1]
This paper is to review the corticosteroid resistant pulmonary fibrosis and how overcome this resistance
The injury of alveolar epithelial cell and apoptosis is followed by type II alveolar cell injury and abnormal lung function, activation of pathways of coagulation, and loss wound healing mechanisms that progressively interrupt lung matrix when fibroblasts are stimulated as epithelial-to-mesenchymal transition (EMT) of alveolar epithelial cells happens, which leading to activation and accumulation of myofibroblasts [90,91,92,93,94]
Summary
The interstitial lung diseases (ILDs) are different classification of lung diseases that are characterized by prolonged inflammation and progressive fibrosis of the pulmonary interstitium [1]. The risk factors of pulmonary fibrosis such as; smoking, gastroesophageal reflux, commonly prescribed drugs such as anti-epileptics, beta blocker (βB), antibiotics, and nonsteroidal antiinflammatory drugs [NSAIDs], diabetes mellitus, environmental exposures, infectious agents and genetic factors [2]
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