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Published on: July 7, 2017
Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders
Sumel Ashique1,2, Neeraj Mishra3, Shubhrajit Mantry4
1Department of Pharmaceutics, Bengal College of Pharmaceutical Sciences & Research, Durgapur, West Bengal, 713212, India. ashiquesumel007@gmail.com.
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.
Insights
Oxidative imbalance drives difficult-to-treat inflammatory lung diseases by causing excessive reactive oxygen species (ROS) and cellular damage. New therapeutic targets are needed to combat this oxidative stress and improve patient outcomes.
Area of Science:
- Pulmonary Medicine
- Oxidative Stress Research
- Inflammatory Diseases
Background:
- Inflammatory lung diseases cause significant global mortality and disability.
- Severe variants of conditions like emphysema, asthma, and COVID-19 lack effective treatments.
- Oxidative imbalance is a key factor in developing challenging inflammatory lung conditions.
Purpose of the Study:
- To highlight the role of oxidative imbalance in severe inflammatory lung disorders.
- To explore the mechanisms linking reactive oxygen species (ROS) to lung tissue damage.
- To identify potential therapeutic targets for oxidative stress-induced lung inflammation.
Main Methods:
- Review of current literature on oxidative stress and inflammatory lung diseases.
- Analysis of the pathways involved in ROS production and signaling.
- Identification of molecular targets for therapeutic intervention.
Main Results:
- Endogenous antioxidant systems are insufficient against induced ROS overproduction.
- ROS triggers pro-inflammatory mediators, leading to tissue damage and worsened inflammation.
- Increased ROS can cause DNA damage, apoptosis, and proto-oncogene activation.
Conclusions:
- Oxidative stress is a critical mechanism in severe inflammatory lung diseases.
- Targeting ROS pathways offers potential for novel therapeutic strategies.
- Further research into these targets could lead to new treatments for intractable lung conditions.
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