There is mounting evidence that targeting mitochondrial dysfunction following neurotrauma could be key in developing effective therapeutic strategies since mitochondria are known to play a major role in cellular bioen...There is mounting evidence that targeting mitochondrial dysfunction following neurotrauma could be key in developing effective therapeutic strategies since mitochondria are known to play a major role in cellular bioenergetics, function, and survival following traumatic spinal cord injury （SCI） （Rabchevsky et al., 2011）. Our research group is one of the pioneers in targeting mitochondrial dysfunction to foster functional neuroprotection, having documented that phar- macological maintenance of mitochondrial function acutely results in long-term neuroprotection and improved function- al recover. We have recently reported that treatment with the pleiotropic drug, pioglitazone, maintains acute mitochondrial integrity correlated with chronic tissue sparing and functional recovery after contusion SCI, but that this was not correlated with altered neuroinflammation （Patel et al., 2017）. We herein propose that the mechanism（s） by which pioglitazone confers neuroprotection may not be entirely dependent upon its activation of peroxisome proliferator activated receptor （PPAR）,展开更多
基金funded by NIH R21NS096670(AGR)Craig H.Neilsen Foundation 476719(AGR)+3 种基金Kentucky Spinal Cord and Head Injury Research Trust#15-14A(PGS)Veterans Affairs Merit Review Award#I01BX003405(PGS)University of Kentucky Spinal Cord and Brain Injury Center Chair Endowments(AGR&PGS)NIH/NINDS 2P30NS051220
文摘There is mounting evidence that targeting mitochondrial dysfunction following neurotrauma could be key in developing effective therapeutic strategies since mitochondria are known to play a major role in cellular bioenergetics, function, and survival following traumatic spinal cord injury （SCI） （Rabchevsky et al., 2011）. Our research group is one of the pioneers in targeting mitochondrial dysfunction to foster functional neuroprotection, having documented that phar- macological maintenance of mitochondrial function acutely results in long-term neuroprotection and improved function- al recover. We have recently reported that treatment with the pleiotropic drug, pioglitazone, maintains acute mitochondrial integrity correlated with chronic tissue sparing and functional recovery after contusion SCI, but that this was not correlated with altered neuroinflammation （Patel et al., 2017）. We herein propose that the mechanism（s） by which pioglitazone confers neuroprotection may not be entirely dependent upon its activation of peroxisome proliferator activated receptor （PPAR）,
