Affiliations 

  • 1 Department of Pharmaceutics, Bengal College of Pharmaceutical Sciences & Research, Durgapur, West Bengal, 713212, India. ashiquesumel007@gmail.com
  • 2 Department of Pharmaceutics, Amity Institute of Pharmacy, Amity University Madhya Pradesh (AUMP), Gwalior, MP, 474005, India
  • 3 Department of Pharmaceutics, Department of Pharmacy, Sarala Birla University, Ranchi, Jharkhand, 835103, India
  • 4 Department of Pharmaceutics, Guru Ramdas Khalsa Institute of Science and Technology (Pharmacy), Jabalpur, Madhya Pradesh, 483001, India
  • 5 SRM Modinagar College of Pharmacy, SRM Institute of Science and Technology (Deemed to Be University), Delhi-NCR Campus, Modinagar, Ghaziabad, Uttar Pradesh, 201204, India
  • 6 Department of Pharmaceutics, Delhi Pharmaceutical Sciences and Research University, Delhi, 110017, India
  • 7 Department of Pharmaceutical Chemistry, Department of Pharmacy, Sarala Birla University, Ranchi, Jharkhand, 835103, India
  • 8 Faculty of Pharmacy, Integral University, Lucknow, Uttar Pradesh, 226026, India
  • 9 Department of Pharmaceutics, Yenepoya Pharmacy College & Research Centre, Yenepoya (Deemed to Be University), Mangalore, Karnataka, 575018, India. mohanto111@gmail.com
  • 10 Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Jalan Lagoon Selatan, Bandar Sunway, 47500, Subang Jaya, Selangor, Malaysia. subramaniyan.vetriselvan@monash.edu
PMID: 39196392 DOI: 10.1007/s00210-024-03392-1

Abstract

A significant number of deaths and disabilities worldwide are brought on by inflammatory lung diseases. Many inflammatory lung disorders, including chronic respiratory emphysema, resistant asthma, resistance to steroids, and coronavirus-infected lung infections, have severe variants for which there are no viable treatments; as a result, new treatment alternatives are needed. Here, we emphasize how oxidative imbalance contributes to the emergence of provocative lung problems that are challenging to treat. Endogenic antioxidant systems are not enough to avert free radical-mediated damage due to the induced overproduction of ROS. Pro-inflammatory mediators are then produced due to intracellular signaling events, which can harm the tissue and worsen the inflammatory response. Overproduction of ROS causes oxidative stress, which causes lung damage and various disease conditions. Invasive microorganisms or hazardous substances that are inhaled repeatedly can cause an excessive amount of ROS to be produced. By starting signal transduction pathways, increased ROS generation during inflammation may cause recurrent DNA damage and apoptosis and activate proto-oncogenes. This review provides information about new targets for conducting research in related domains or target factors to prevent, control, or treat such inflammatory oxidative stress-induced inflammatory lung disorders.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.