Dr Gianmichele Massimo
Postdoctoral Researcher
Centre for Cardiovascular Medicine and Devices (WHRI)
Queen Mary University of London
Queen Mary University of London
Research
My research activity aims to understand how genetic mutations of xanthine oxidoreductase enzyme (XOR), the rate-limiting enzyme of purines (hypoxanthine, xanthine) metabolism, affect its activity in terms of uric acid, reactive oxygen species and nitric oxide production.
Interests
My research activity aims to understand whether genetic mutations of xanthine oxidoreductase enzyme (XOR), altering its structure, expression and activity, have a role in the development of endothelial dysfunction and ultimately in cardiovascular disease. There are numerous evidence supporting the concept that raised levels of circulating UA represent an independent risk factor for cardiovascular diseases (like heart failure), as well as numerous evidence showing that under pathophysiological conditions, such as ischemia-reperfusion, hypertension, atherosclerosis, diabetes, XOR activity and expression are upregulated. There is also some evidence suggesting that non-synonymous genetic mutations of XDH alter its expression and activity. To investigate how this mutations modulate the expression, the tertiary structure and its activity, I have developed a 2D in vitro model of WT and mutated hXOR HEK-293 cells.Publications
2021
Gee LC, Massimo G, Lau C, Primus C, Fernandes D, Chen J, Rathod KS, Hamers AJP, Filomena F, Nuredini G, Ibrahim AS, Khambata RS, Gupta AK, Moon JC, Kapil V and Ahluwalia A (2021). Inorganic nitrate attenuates cardiac dysfunction: roles for xanthine oxidoreductase and nitric oxide. Wiley British Journal of Pharmacology vol. 179, (20) 4757-4777.
2020
Kapil V, Khambata RS, Jones DA, Rathod K, Primus C, Massimo G, Fukuto JM and Ahluwalia A (2020). The Noncanonical Pathway for In Vivo Nitric Oxide Generation: The Nitrate-Nitrite-Nitric Oxide Pathway. Pharmacological reviews vol. 72, (3) 692-766.
2018
Chen J, Hamers AJP, Finsterbusch M, Massimo G, Zafar M, Corder R, Colas RA, Dalli J, Thiemermann C and Ahluwalia A (2018). Endogenously generated arachidonate-derived ligands for TRPV1 induce cardiac protection in sepsis. FASEB J fj201701303-fj201701303.