Therapeutic effect of statins on airway remodeling during asthma

ABSTRACT

Introduction

Asthma is a chronic inflammatory disease of the airways, which is usually characterized by remodeling, hyperresponsiveness and episodic obstruction of the airways. The underlying chronic airway inflammation leads to pathological restructuring of both the large and small airways. Since the effects of current asthma medications on airway remodeling have been met with contradictions, many therapeutic agents have been redirected from their primary use for the treatment of asthma. Such treatments, which could target several signaling molecules implicated in the inflammatory and airway remodeling processes of asthma, would be an ideal choice.

Areas covered

Statins are effective serum cholesterol-lowering agents that were found to have potential anti-inflammatory and anti-remodeling properties. Literature search was done for the past 10 years to include research and review articles in the field of statins and asthma complications. In this review, we discuss the role of statins in airway tissue remodeling and their potential therapeutic modalities in asthma.

Expert Opinion

With improved understanding of the role of statins in airway remodeling and inflammation, statins represent a potential therapeutic option for various asthma phenotypes. Further research is warranted to optimize statins for asthma therapy through inhalation as a possible route of administration.

KEYWORDS:

• Statins
• airway remodeling
• asthma
• inflammation
• therapeutics

Article highlights

• Statins may reduce airway inflammation and remodeling in asthmatics.

• Statins act on several immune and non-immune cells, which play key roles in the pathophysiology of asthma.

• Immuno-modulating and anti-remodeling properties of statins shed new light on their promising use in the treatment of asthma.

Declaration of Interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

The manuscript was funded by Tissue Injury and Repair (TIR) group operational grant (Grant code: 150317); COVID-19 research grant (CoV19-0307), Seed grant (Grant code: 2001090275); and by collaborative research grant (Grant code: 2001090278) to RH, University of Sharjah, UAE; and by a Sandooq Al Watan Applied Research & Development grant to RH (SWARD-S20-007), UAE; and by Al Jalila Foundation Seed Grant to RH (AJF202019), UAE.