Mitochondria-Targeting Particles

Abstract

Mitochondria are a promising therapeutic target for the detection, prevention and treatment of various human diseases such as cancer, neurodegenerative diseases, ischemia-reperfusion injury, diabetes and obesity. To reach mitochondria, therapeutic molecules need to not only gain access to specific organs, but also to overcome multiple barriers such as the cell membrane and the outer and inner mitochondrial membranes. Cellular and mitochondrial barriers can be potentially overcome through the design of mitochondriotropic particulate carriers capable of transporting drug molecules selectively to mitochondria. These particulate carriers or vectors can be made from lipids (liposomes), biodegradable polymers, or metals, protecting the drug cargo from rapid elimination and degradation in vivo. Many formulations can be tailored to target mitochondria by the incorporation of mitochondriotropic agents onto the surface and can be manufactured to desired sizes and molecular charge. Here, we summarize recently reported strategies for delivering therapeutic molecules to mitochondria using various particle-based formulations.

Keywords::

• intracellular targeting
• mitochondria
• mitochondria targeting
• nanotechnology
• organelle specific
• particles

Financial & competing interests disclosure

The authors gratefully acknowledge support from the American Cancer Society (RSG-09–015–01-CDD), the National Cancer Institute at the NIH (1R21CA13345-01/1R21CA128414-01A2/UI Mayo Clinic Lymphoma SPORE), and the Lyle and Sharon Bighley Professorship. A Wongrakpanich acknowledges support from the Royal Thai Government Scholarship. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors gratefully acknowledge support from the American Cancer Society (RSG-09–015–01-CDD), the National Cancer Institute at the NIH (1R21CA13345-01/1R21CA128414-01A2/UI Mayo Clinic Lymphoma SPORE), and the Lyle and Sharon Bighley Professorship. A Wongrakpanich acknowledges support from the Royal Thai Government Scholarship. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.