Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis.
J, J., Y, K., SJ, S., Y, J., JY, A., & M, S. (2026). Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis.. ACS nano. https://doi.org/10.1021/acsnano.6c05982
J J, Y K, SJ S, Y J, JY A, M S. Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis.. ACS nano. 2026; doi: 10.1021/acsnano.6c05982
J J, Y K, SJ S, et al. Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis.[J]. ACS nano. 2026. DOI: 10.1021/acsnano.6c05982.
@article{j2026,
author = {Ju J and Kim Y and Seo SJ and Jin Y and Ahn JY and Shin M},
title = {Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis.},
journal = {ACS nano},
year = {2026},
doi = {10.1021/acsnano.6c05982},
note = {PMID: 42579408},
}
TY - JOUR AU - Ju J AU - Kim Y AU - Seo SJ AU - Jin Y AU - Ahn JY AU - Shin M TI - Adenosine Triphosphate Nanoparticles with Blood-Brain Barrier Permeability for Prevention of Cerebral Ischemic Injury via Mitochondrial Homeostasis. T2 - ACS nano PY - 2026 DO - 10.1021/acsnano.6c05982 AN - PMID:42579408 ER -
Cerebral ischemia induces selective neuronal death, largely due to mitochondrial dysfunction and ATP depletion. This energy crisis impairs mitophagy, exacerbates oxidative stress, and accelerates neuronal apoptosis. While exogenous ATP supplementation holds promise for restoring mitochondrial function, its clinical application is hindered by rapid in vivo clearance before brain accumulation occurs. Herein, we report positively charged ATP nanoparticles (ATP-N), formulated via electrostatic interactions with chitosan, that facilitate crossing the blood-brain barrier and subsequent adsorptive-mediated transcytosis following intravenous injection, for the prevention of cerebral ischemic injury. Compared with free ATP, ATP-N exhibited a prolonged circulation time and enhanced brain accumulation. In a mouse model of cerebral ischemia, ATP-N effectively replenished intracellular ATP, restored mitochondrial membrane potential, and activated mitophagy, leading to reduced neuronal apoptosis and attenuated ischemic damage. These findings highlight ATP-N as a promising, minimally invasive therapeutic strategy to prevent ischemic brain injury, enabling rapid and efficient ATP delivery to restore mitochondrial function and promote neuronal survival.