Professor Syed E A Haq MB BS BSc (HON) PhD DIC MRCP(UK)
Professor Syed Haq, is a Consultant Physician and Founder of The London Preventative Medicine Centre. He is the Clinical and Scientific Director of Daval International Ltd., a biopharmaceutical company developing a platform for the treatment of autoimmune (e.g., Systemic Sclerosis), neurodegenerative (e.g., Motor neuron disease, Alzheimer’s disease, Myasthenia Gravis, Multiple Sclerosis) and inflammatory (e.g., Rheumatoid arthritis) diseases using a patented polyclonal antibody/peptide composite which has recently completed two phase II clinical trials in the UK. He has worked and trained at some of the foremost institutions - Guy’s Hospital, Hammersmith and Royal Brompton Hospitals, Imperial College, Massachusetts General Hospital, Harvard Medical School, and Tufts University, New England Medical Center Hospitals Inc.

Prof. Haq has published peer-reviewed articles in several internationally renowned scientific journals including PNAS and Nature Medicine. He has been co-chairman of the Anti-ageing Conference London (2008-11), and has been an invited presenter/speaker at numerous international conferences (American Heart Association, American College of Cardiology, Anti-Ageing Medicine World Congress and the NCD National Workshop, India). Prof. Haq has received several national and international awards/fellowships from the Medical Research Council, Wellcome Trust International, American Heart Association, Astra Zeneca and the Heart Failure Society of America.

2008 - Cytosolic Phospholipase A2 is fundamental in regulating insulin-like growth factor-1 mediated signalling and mammalian growth.

Phospholipase A2s comprise a family of enzymes that act at the sn-2 position of phospholipids (PLs), generating a free fatty acid and lysophospholipid. As the sn-2 position of PLs is enriched with arachidonic acid (AA), an eicosanoid precursor, PLA2 activity has important implications for the control of eicosanoid production. The 85 kDa cytosolic PLA2 (c-PLA2) plays a central role in AA release and eicosanoid generation. Based on in vivo studies, generation of AA by the ubiquitously expressed cytosolic phospholipase A2 (PLA2) plays a fundamental role in the regulation of cellular homeostasis, normal parturition, inflammation, and tumourigenesis. In our studies we report that cytosolic PLA2 is a negative regulator of growth, specifically of striated muscle. We find that normal growth of skeletal muscle, and normal and pathologic stress-induced hypertrophic growth of the heart are exaggerated in a mouse deleted for the gene encoding cytosolic PLA2. Evidence suggests that the physiologically relevant activator of the pathway that regulates normal post-natal growth is insulin-like growth factor-1 (IGF-1), acting via its receptor and the insulin receptor substrate-1 (IRS-1). IGF-1 signalling has also been implicated in pathologic stress-induced hypertrophic growth of the heart. The mechanism underlying the exaggerated growth phenotype is that cytosolic PLA2 negatively regulates IGF-1 signalling. Absence of cytosolic PLA2 leads to sustained activation of the IGF-1 pathway, which results from 3’-phosphoinositide-dependent kinase-1 (PDK1’s) failure to recruit and phosphorylate protein kinase C z, a negative regulator of IGF-1 signalling. Importantly, AA restores activation of PKC z, correcting the exaggerated IGF-1 signalling. In conclusion, these results have important implications for normal mammalian growth and ageing. They indicate that cytosolic PLA2 and AA critically regulate striated muscle growth by modulating multiple growth regulatory pathways. The findings identify a novel role for cytosolic PLA2 as a negative regulator both of IGF-1 signalling, and of normal and pathologic growth of striated muscle