Mukundan G. Attur, PhD

My work is dedicated to uncovering the complexities of osteoarthritis (OA), challenging its traditional classification as a non-inflammatory disease. Starting from my early studies on inflammatory mediators in OA cartilage, my research has pioneered new understanding and treatment methods for this condition.

As a research associate from 1998 to 2001, I applied genomics and proteomics to investigate the autocrine and paracrine mechanisms of IL-1β in chondrocytes. We developed gene therapy approaches for OA cartilage repair and standardized RNA and protein isolation protocols for gene and protein profiling.

Over the years, I’ve developed gene therapy approaches for cartilage repair, standardized protocols for profiling gene and protein expressions, and discovered key biomarkers in OA. My research has been crucial in highlighting the role of low-grade inflammation in the progression of knee OA and identifying genetic variations in the IL-1 gene family that predict disease severity. Throughout my career, I've challenged the traditional classification of OA as a non-inflammatory disease. My early research revealed that OA cartilage produces several inflammatory mediators, including nitric oxide, eicosanoids, cytokines, chemokines, and matrix metalloproteinases (MMPs). These findings were pivotal in reshaping the understanding of OA and its treatment.

Recent collaborations include research on genicular artery embolization (GAE) as a disease-modifying treatment for knee OA and the impact of IL1RN genetic variants on cytokine storms and disease severity in SARS-CoV-2 patients. I also established the Arthritis Biobank and co-founded the Microbiome Center for Rheumatology and Autoimmunity (MiCRA), supporting multiple projects. My translational studies have demonstrated the impact of low-grade inflammation and IL1RN gene variations on OA progression, showing that specific genetic polymorphisms in the IL1RN gene predict age-related OA severity and risk for incident knee OA.

During the COVID-19 pandemic, my work on genetic variations in the IL1RN gene provided insights into protection against severe illness from cytokine storms and further studies on post-acute sequelae of SARS-CoV-2. Moving forward, my focus remains on identifying molecular pathways and validating biomarkers to advance our understanding of arthritis and other inflammatory diseases.