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Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Reactive Oxygen Species-Mediated Mitochondrial-Targeted Therapeutics in Hepatic Disorders: Current Progress and
Ashish Dhiman1, Yagni Shah1, Umesh Chaudhary1
1Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research-Ahmedabad (NIPER-A), Opposite Airforce Station, Palaj, Gandhinagar, Gujarat 382355, India.
Abstract:
Reactive oxygen species (ROS) are key mediators of mitochondrial dysfunction, contributing to the onset and development of hepatic disorders, including nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and liver fibrosis. Mitochondria, as central regulators of cellular energy and metabolism, are both sources and targets of ROS, making them critical in understanding liver disease pathology. Current approaches include the development of mitochondria-specific antioxidants, therapeutic agents that enhance mitochondrial biogenesis, and nanotechnology-based delivery systems to improve precision targeting. Emerging approaches such as the modulation of mitochondrial dynamics and mitophagy hold significant potential to restore mitochondrial function and cellular homeostasis. The various causes of mitochondrial dysfunction, with a focus on ROS involvement in the pathogenesis of hepatic disorders, are discussed. Here, currently explored therapeutic remedies for mitochondrial dysfunction and their potential in translating them into clinical applications are covered. A discussion of recent advances in mitochondrial-targeted therapeutics for hepatic disorders is also included. The review concludes by identifying promising directions for future research, emphasizing the need for innovative strategies to exploit the interplay between ROS and mitochondrial dysfunction. These advances could pave the way for targeted, effective therapies for managing hepatic disorders.
Insights
Reactive oxygen species (ROS) drive mitochondrial dysfunction in liver diseases like NAFLD and ALD. Targeting ROS and mitochondria offers promising therapeutic strategies for hepatic disorders.
Area of Science:
- Mitochondrial biology and pathophysiology
- Hepatology and liver disease research
- Oxidative stress and cellular signaling
Background:
- Mitochondrial dysfunction, driven by reactive oxygen species (ROS), is central to liver diseases such as nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and liver fibrosis.
- Mitochondria are both sources and targets of ROS, highlighting their critical role in liver disease pathogenesis and cellular energy regulation.
Purpose of the Study:
- To review the causes of mitochondrial dysfunction, emphasizing the role of ROS in hepatic disorders.
- To discuss current and emerging therapeutic strategies targeting mitochondrial dysfunction for liver diseases.
- To explore recent advances in mitochondrial-targeted therapeutics and their clinical potential.
Main Methods:
- Literature review of studies on mitochondrial dysfunction, ROS, and hepatic disorders.
- Analysis of current therapeutic approaches including antioxidants, biogenesis enhancers, and nanotechnology.
- Examination of emerging strategies like mitochondrial dynamics modulation and mitophagy.
Main Results:
- Reactive oxygen species (ROS) are significant contributors to mitochondrial dysfunction in various hepatic disorders.
- Mitochondria-specific antioxidants, enhanced mitochondrial biogenesis, and targeted delivery systems are key therapeutic avenues.
- Modulating mitochondrial dynamics and mitophagy presents novel therapeutic potential for restoring cellular homeostasis.
Conclusions:
- Targeting the interplay between ROS and mitochondrial dysfunction is crucial for developing effective therapies for hepatic disorders.
- Translating current and emerging mitochondrial-targeted strategies into clinical applications holds significant promise for managing liver diseases.
- Future research should focus on innovative approaches to exploit mitochondrial pathways for treating liver conditions.
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