Mitochondria and neuroprotection in stroke: Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics

Gabriella MacDougall, Ryan S. Anderton, Frank L. Mastaglia, Neville W. Knuckey, Bruno P. Meloni

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Stroke is the second leading cause of death globally and represents a major cause of devastating long-term disability. Despite sustained efforts to develop clinically effective neuroprotective therapies, presently there is no clinically available neuroprotective agent for stroke. As a central mediator of neurodamaging events in stroke, mitochondria are recognised as a critical neuroprotective target, and as such, provide a focus for developing mitochondrial-targeted therapeutics. In recent years, cationic arginine-rich peptides (CARPs) have been identified as a novel class of neuroprotective agent with several demonstrated mechanisms of action, including their ability to target mitochondria and exert positive effects on the organelle. This review provides an overview on neuronal mitochondria] dysfunction in ischaemic stroke pathophysiology and highlights the potential beneficial effects of CARPs on mitochondria in the ischaemic brain following stroke.

Original languageEnglish
Pages (from-to)17-33
Number of pages17
JournalNeurobiology of Disease
Volume121
DOIs
Publication statusPublished - Jan 2019

Cite this

@article{ef1ef13d42ce47beaa565dc086a1213d,
title = "Mitochondria and neuroprotection in stroke: Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics",
abstract = "Stroke is the second leading cause of death globally and represents a major cause of devastating long-term disability. Despite sustained efforts to develop clinically effective neuroprotective therapies, presently there is no clinically available neuroprotective agent for stroke. As a central mediator of neurodamaging events in stroke, mitochondria are recognised as a critical neuroprotective target, and as such, provide a focus for developing mitochondrial-targeted therapeutics. In recent years, cationic arginine-rich peptides (CARPs) have been identified as a novel class of neuroprotective agent with several demonstrated mechanisms of action, including their ability to target mitochondria and exert positive effects on the organelle. This review provides an overview on neuronal mitochondria] dysfunction in ischaemic stroke pathophysiology and highlights the potential beneficial effects of CARPs on mitochondria in the ischaemic brain following stroke.",
keywords = "Stroke, Ischaemia, Cationic arginine-rich peptides, Mitochondria, Mito-protection, Oxidative stress, Membrane potential, Permeability transition, Apoptosis, CELL-PENETRATING PEPTIDES, ISCHEMIC BRAIN-INJURY, FOCAL CEREBRAL-ISCHEMIA, PROTECTS HIPPOCAMPAL-NEURONS, PERMEABILITY TRANSITION PORE, SUBSEQUENT DNA FRAGMENTATION, APOPTOSIS-INDUCING FACTOR, AP-1 INHIBITORY PEPTIDES, NA-1 TAT-NR2B9C PEPTIDES, NITRIC-OXIDE SYNTHASE",
author = "Gabriella MacDougall and Anderton, {Ryan S.} and Mastaglia, {Frank L.} and Knuckey, {Neville W.} and Meloni, {Bruno P.}",
year = "2019",
month = "1",
doi = "10.1016/j.nbd.2018.09.010",
language = "English",
volume = "121",
pages = "17--33",
journal = "Neurobiology of Disease",
issn = "0969-9961",
publisher = "Academic Press",

}

TY - JOUR

T1 - Mitochondria and neuroprotection in stroke

T2 - Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics

AU - MacDougall, Gabriella

AU - Anderton, Ryan S.

AU - Mastaglia, Frank L.

AU - Knuckey, Neville W.

AU - Meloni, Bruno P.

PY - 2019/1

Y1 - 2019/1

N2 - Stroke is the second leading cause of death globally and represents a major cause of devastating long-term disability. Despite sustained efforts to develop clinically effective neuroprotective therapies, presently there is no clinically available neuroprotective agent for stroke. As a central mediator of neurodamaging events in stroke, mitochondria are recognised as a critical neuroprotective target, and as such, provide a focus for developing mitochondrial-targeted therapeutics. In recent years, cationic arginine-rich peptides (CARPs) have been identified as a novel class of neuroprotective agent with several demonstrated mechanisms of action, including their ability to target mitochondria and exert positive effects on the organelle. This review provides an overview on neuronal mitochondria] dysfunction in ischaemic stroke pathophysiology and highlights the potential beneficial effects of CARPs on mitochondria in the ischaemic brain following stroke.

AB - Stroke is the second leading cause of death globally and represents a major cause of devastating long-term disability. Despite sustained efforts to develop clinically effective neuroprotective therapies, presently there is no clinically available neuroprotective agent for stroke. As a central mediator of neurodamaging events in stroke, mitochondria are recognised as a critical neuroprotective target, and as such, provide a focus for developing mitochondrial-targeted therapeutics. In recent years, cationic arginine-rich peptides (CARPs) have been identified as a novel class of neuroprotective agent with several demonstrated mechanisms of action, including their ability to target mitochondria and exert positive effects on the organelle. This review provides an overview on neuronal mitochondria] dysfunction in ischaemic stroke pathophysiology and highlights the potential beneficial effects of CARPs on mitochondria in the ischaemic brain following stroke.

KW - Stroke

KW - Ischaemia

KW - Cationic arginine-rich peptides

KW - Mitochondria

KW - Mito-protection

KW - Oxidative stress

KW - Membrane potential

KW - Permeability transition

KW - Apoptosis

KW - CELL-PENETRATING PEPTIDES

KW - ISCHEMIC BRAIN-INJURY

KW - FOCAL CEREBRAL-ISCHEMIA

KW - PROTECTS HIPPOCAMPAL-NEURONS

KW - PERMEABILITY TRANSITION PORE

KW - SUBSEQUENT DNA FRAGMENTATION

KW - APOPTOSIS-INDUCING FACTOR

KW - AP-1 INHIBITORY PEPTIDES

KW - NA-1 TAT-NR2B9C PEPTIDES

KW - NITRIC-OXIDE SYNTHASE

U2 - 10.1016/j.nbd.2018.09.010

DO - 10.1016/j.nbd.2018.09.010

M3 - Review article

VL - 121

SP - 17

EP - 33

JO - Neurobiology of Disease

JF - Neurobiology of Disease

SN - 0969-9961

ER -