Chandelier
Senior Member (Voting Rights)
Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency
Cells naturally transfer mitochondria to help repair damage, but this process is inefficient.
Here, we use molybdenum disulfide (MoS2) nanoflowers to boost mitochondrial production, turning donor cells into mitochondrial biofactories.
These cells transfer more mitochondria to damaged cells, significantly improving energy production and function.
In disease models, this approach restores cell health, offering a strategy for treating mitochondrial-related disorders.
By enhancing the body’s own repair mechanisms, this nanomaterial-based method could pave the way for innovative therapies in regenerative medicine.
Enhancing this natural process holds promise for developing novel therapies targeting diseases associated with mitochondrial dysfunction.
Here, we introduce a nanomaterial-based approach employing molybdenum disulfide (MoS2) nanoflowers with atomic-scale vacancies to stimulate mitochondrial biogenesis in cells to make them mitochondrial biofactories.
Upon cellular uptake, these nanoflowers result in a two-fold increase in mitochondrial mass and enhancing mitochondrial transfer to recipient cells by several-fold. This enhanced efficiency of transfer significantly improves mitochondrial respiratory capacity and adenosine triphosphate production in recipient cells under physiological conditions. In cellular models of mitochondrial and cellular damage, MoS2 enhanced mitochondrial transfer achieved remarkable restoration of cell function.
This proof-of-concept study demonstrates that nanomaterial-boosted intercellular mitochondrial transfer can enhance cell survivability and function under diseased conditions, offering a promising strategy for treating mitochondrial dysfunction-related diseases.
Web | DOI | PMC | PDF | Proceedings of the National Academy of Sciences
Soukar, John; Singh, Kanwar Abhay; Aviles, Ari; Hargett, Sarah; Kaur, Harman; Foster, Samantha; Roy, Shounak; Zhao, Feng; Gohil, Vishal M.; Singh, Irtisha; Gaharwar, Akhilesh K.
Significance
Mitochondrial dysfunction plays a key role in many diseases, yet treatments to restore function remain limited.Cells naturally transfer mitochondria to help repair damage, but this process is inefficient.
Here, we use molybdenum disulfide (MoS2) nanoflowers to boost mitochondrial production, turning donor cells into mitochondrial biofactories.
These cells transfer more mitochondria to damaged cells, significantly improving energy production and function.
In disease models, this approach restores cell health, offering a strategy for treating mitochondrial-related disorders.
By enhancing the body’s own repair mechanisms, this nanomaterial-based method could pave the way for innovative therapies in regenerative medicine.
Abstract
Intercellular mitochondrial transfer, the spontaneous exchange of mitochondria between cells, is a recently described phenomenon crucial for cellular repair, regeneration, and disease management.Enhancing this natural process holds promise for developing novel therapies targeting diseases associated with mitochondrial dysfunction.
Here, we introduce a nanomaterial-based approach employing molybdenum disulfide (MoS2) nanoflowers with atomic-scale vacancies to stimulate mitochondrial biogenesis in cells to make them mitochondrial biofactories.
Upon cellular uptake, these nanoflowers result in a two-fold increase in mitochondrial mass and enhancing mitochondrial transfer to recipient cells by several-fold. This enhanced efficiency of transfer significantly improves mitochondrial respiratory capacity and adenosine triphosphate production in recipient cells under physiological conditions. In cellular models of mitochondrial and cellular damage, MoS2 enhanced mitochondrial transfer achieved remarkable restoration of cell function.
This proof-of-concept study demonstrates that nanomaterial-boosted intercellular mitochondrial transfer can enhance cell survivability and function under diseased conditions, offering a promising strategy for treating mitochondrial dysfunction-related diseases.
Web | DOI | PMC | PDF | Proceedings of the National Academy of Sciences