TY - JOUR
T1 - Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach
AU - Ahluwalia, Meenakshi
AU - Kumar, Manish
AU - Ahluwalia, Pankaj
AU - Rahimi, Scott
AU - Vender, John R.
AU - Raju, Raghavan P.
AU - Hess, David C.
AU - Baban, Babak
AU - Vale, Fernando L.
AU - Dhandapani, Krishnan M.
AU - Vaibhav, Kumar
N1 - Publisher Copyright:
© 2021
PY - 2021/11
Y1 - 2021/11
N2 - Mitochondria are dynamic organelles responsible for cellular energy production. Besides, regulating energy homeostasis, mitochondria are responsible for calcium homeostasis, signal transmission, and the fate of cellular survival in case of injury and pathologies. Accumulating reports have suggested multiple roles of mitochondria in neuropathologies, neurodegeneration, and immune activation under physiological and pathological conditions. Mitochondrial dysfunction, which occurs at the initial phase of brain injury, involves oxidative stress, inflammation, deficits in mitochondrial bioenergetics, biogenesis, transport, and autophagy. Thus, development of targeted therapeutics to protect mitochondria may improve functional outcomes following traumatic brain injury (TBI) and intracerebral hemorrhages (ICH). In this review, we summarize mitochondrial dysfunction related to TBI and ICH, including the mechanisms involved, and discuss therapeutic approaches with special emphasis on past and current clinical trials.
AB - Mitochondria are dynamic organelles responsible for cellular energy production. Besides, regulating energy homeostasis, mitochondria are responsible for calcium homeostasis, signal transmission, and the fate of cellular survival in case of injury and pathologies. Accumulating reports have suggested multiple roles of mitochondria in neuropathologies, neurodegeneration, and immune activation under physiological and pathological conditions. Mitochondrial dysfunction, which occurs at the initial phase of brain injury, involves oxidative stress, inflammation, deficits in mitochondrial bioenergetics, biogenesis, transport, and autophagy. Thus, development of targeted therapeutics to protect mitochondria may improve functional outcomes following traumatic brain injury (TBI) and intracerebral hemorrhages (ICH). In this review, we summarize mitochondrial dysfunction related to TBI and ICH, including the mechanisms involved, and discuss therapeutic approaches with special emphasis on past and current clinical trials.
KW - Brain injury
KW - Immune activation
KW - Mitochondrial bioenergetics
KW - Mitochondrial biogenesis
KW - Mitophagy
KW - Therapeutic approach
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U2 - 10.1016/j.neuint.2021.105192
DO - 10.1016/j.neuint.2021.105192
M3 - Article
C2 - 34560175
AN - SCOPUS:85115783465
SN - 0197-0186
VL - 150
JO - Neurochemistry International
JF - Neurochemistry International
M1 - 105192
ER -