HYBRID EVENT: You can participate in person at Rome, Italy or Virtually from your home or work.

4th Edition of Euro-Global Conference on Biotechnology and Bioengineering

September 19-21 | Hybrid Event

September 19-21, 2024 | Rome, Italy
ECBB 2024

Molecular therapeutics for chronic obstructive pulmonary disease

Yong Xiao Wang, Speaker at Bioengineering Conferences
Albany Medical College, United States
Title: Molecular therapeutics for chronic obstructive pulmonary disease

Abstract:

Chronic obstructive pulmonary disease (COPD) is a devastating common lung disease. It is the third leading cause of mortality in the world and will be the second leading cause of death by 2020. The current challenging tasks are that the molecular mechanisms for COPD remain largely unknown, and clinical therapeutic options are limited. A major characteristic of COPD is expiratory airflow limitation, which can be attributed to airway hyperresponsiveness and remodeling. We and other well-known scientist have unveiled that a very important player (VIP) in these two major cellular responses is an increase in intracellular calcium ([Ca2+]i) in airway smooth muscle cells (AMCs). Consistent with this view, bronchodilators including muscarinic receptor antagonists, β-adrenergic receptor agonists and corticosteroids are used as the first-line drugs in the clinical treatment of COPD, and the functional role of all these forefront drugs are associated with their inhibition of the increased [Ca2+]i in ASMCs. Recent studies from our group and others suggest that multiple ion channels, particularly inositol trisphosphate receptor (IP3R)/Ca2+ release channel, ryanodine receptor (RyR)/Ca2+ release channel and canonical transient receptor potential-3 (TRPC3) channel, play a major role in initiation and maintenance of [Ca2+]i in ASMCs and thus are essential for airway hyperresponsiveness and remodeling in COPD and/or other pulmonary diseases. Equally interestingly, IP3R, RyR and TRPC3 channels are highly sensitive to reactive oxygen species (ROS), and ROS are well known to mediate airway hyperresponsiveness and/or remodeling in COPD. We have further reveal that ROS are primarily produced by mitochondria and NADPH oxidase (NOX), but mitochondria are the primary site. Several antioxidants targeted at mitochondria and/or NOX are currently used in clinical trials and show potential effectiveness in the treatment of COPD. ROS may implement their roles in COPD by causing oxidation of IP3R, RyR and TRPC3 channels, leading to their hyperfunctions. We and other eminent investigators have further provided new evidence that virus-mediated shRNA-based genetic (specific) inhibition and highly selective pharmacological inhibitor of these channels may become more effective therapies for COPD.

Biography:

Yong Xiao Wang has been a Full Professor in Department of Molecular and Cellular Physiology at Albany Medical College since 2006. Dr. Wang obtained his MD at Wannan Medical University, PhD at Fourth Military Medical University, and postdoctoral training at Technology University of Munich and University of Pennsylvania. He has made many important findings using complementary molecular, biochemical, physiological, and genetic approaches at the molecular, organelle, cellular, tissue and organism levels in animals and human samples, had numerous publications in Nature Commun (impact factor: 17.694), Antioxid Redox Signal (8.401), Proc Natl Acad Sci USA (12.779), Nature (69.504), Circ Res (23.218), and other highly peer-reviewed journals and academic books, and served as the editorial board member and/or section editor as well as the executive committee member and/or subcommittee chair for professional societies.

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