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Epigenetics in Asthma

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Targeting Epigenetics in Inflammatory Lung Diseases

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Abstract

Asthma is one of the highest incidences and disbursed respiratory diseases the world over. There is incomprehensible knowledge of pathophysiological epigenetic pathways and causal interaction in asthma. Hereby, with a focus on DNA methylation, we examine human investigations on the epigenetic processes of asthma. On analysis, it was found that epigenetic research on childhood asthma has uncovered distinct methylation profiles linked to allergic inflammation in immune cells and the airways, demonstrating that methylation plays a regulatory function in the pathogenesis of asthma. Considering these ground-breaking findings, additional research is needed to understand how epigenetic pathways contribute to the endotypes of asthma. Studies on histone alterations in asthma are very few. Future investigations into the epigenetic causes of asthma will be aided by the inclusion of data from groups with accurate phenotyping.

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Author information

Authors and Affiliations

  1. Department of Pharmacology, College of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia

    Waleed Hassan Almalki

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  1. Waleed Hassan Almalki
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Editors and Affiliations

  1. School of Pharmacy, Suresh Gyan University, Jaipur, Rajasthan, India

    Gaurav Gupta

  2. Department of Science, University of Technology Sydney, Ultimo, NSW, Australia

    Brian G. Oliver

  3. Discipline of Pharmacy, University of Technology Sydney, Schofields, NSW, Australia

    Kamal Dua

  4. Division of Pulmonary and Critical Care Medicine, Stanford Medicine, Stanford, CA, USA

    Md Khadem Ali

  5. School of Pharmacy, Gyan Vihar University, Jaipur, Rajasthan, India

    Piyush Dave

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© 2023 The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.

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Almalki, W.H. (2023). Epigenetics in Asthma. In: Gupta, G., Oliver, B.G., Dua, K., Ali, M.K., Dave, P. (eds) Targeting Epigenetics in Inflammatory Lung Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-99-4780-5_5

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