Review Article Peroxisome proliferator activated receptor-γ and traumatic brain injury
Lei Qi, Asha Jacob, Ping Wang, Rongqian Wu
Department of Surgery, North Shore University Hospital and Long Island Jewish Medical Center, Manhasset, NY 11030, USA; The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA; Department of Neurosurgery, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China
Received August 6, 2010; accepted September 18, 2010; available online September 23, 2010
Abstract: Traumatic brain injury (TBI) represents a major health care problem and a significant socioeconomic challenge worldwide. No specific therapy for TBI is available. The peroxisome proliferator activated receptor-γ (PPAR-γ) belongs to the nuclear receptor superfamily. Although PPAR-γ was originally characterized in adipose tissue as a regulator of lipid and glucose metabolism, recent studies showed that PPAR-γ is present in most cell types and plays a central role in the regulation of adipogenesis, glucose homeostasis, cellular differentiation, apoptosis and inflammation. Here, we reviewed the current literature on the molecular mechanisms of PPAR-γ-related neuroprotection after TBI. Growing evidence has indicated that the beneficial effects of PPAR-γ activation in TBI appear to be mediated through downregulation of inflammatory responses, reduction of oxidative stress, inhibition of apoptosis, and promotion of neurogenesis. A thorough understanding of the PPAR-γ pathway will be critical to the development of therapeutic interventions for the treatment of patients with TBI. (IJCEM1008001).
Address all correspondence to: Rongqian Wu, MD, PhD Laboratory of Surgical Research The Feinstein Institute for Medical Research 350 Community Drive Manhasset, NY 11030 Tel: (516) 562-2390 Fax: (516) 562-2396 E-mail: email@example.com