Mitochondria-Targeted Drug Delivery

Review Pharmacology & Pharmacy

Protective Effect of Mitochondria-Targeted Antioxidants against Inflammatory Response to Lipopolysaccharide Challenge: A Review

Ekaterina M. Fock et al.

Summary: Lipopolysaccharide (LPS) challenge leads to oxidative stress and mitochondrial dysfunction, causing cell and tissue damage. Mitochondrial reactive oxygen species (mtROS) play a key role in inflammation, with excessive levels impairing mitochondrial function and causing oxidative damage. Mitochondria-targeted antioxidants (mito-AOX) have shown promise in protecting against LPS-induced damage and developing new treatment strategies for Gram-negative infections.

PHARMACEUTICS (2021)

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Article Pharmacology & Pharmacy

Effect of Diphenyleneiodonium Chloride on Intracellular Reactive Oxygen Species Metabolism with Emphasis on NADPH Oxidase and Mitochondria in Two Therapeutically Relevant Human Cell Types

Sergejs Zavadskis et al.

Summary: The study found that the inhibitor DPI has different effects on ROS metabolism and mitochondrial function in various types of cells, such as stem cells and differentiated cells, depending on the cell's energy metabolism. Undifferentiated cells may be a better target for DPI compared to differentiated parenchymal cells.

PHARMACEUTICS (2021)

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Article Pharmacology & Pharmacy

Chimeric Drug Design with a Noncharged Carrier for Mitochondrial Delivery

Consuelo Ripoll et al.

Summary: This study confirms the general applicability of the thiophene group as a mitochondrial carrier for drugs and fluorescent markers based on a new concept of nonprotonable, noncharged transporter. The promising features of the thiophene moiety as a noncharged carrier for targeting mitochondria may represent a starting point for the design of new metabolism-targeting drugs.

PHARMACEUTICS (2021)

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Article Pharmacology & Pharmacy

Plumbagin Elicits Cell-Specific Cytotoxic Effects and Metabolic Responses in Melanoma Cells

Haoran Zhang et al.

Summary: The study reveals the relationship between metabolism and cytotoxic effects of PLB in melanoma, indicating PLB displays stronger cytotoxic effects on A375 cells and triggers cell-specific metabolic changes in accordance with its cytotoxic effects.

PHARMACEUTICS (2021)

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Review Pharmacology & Pharmacy

Engineering Genetic Systems for Treating Mitochondrial Diseases

Yoon-ha Jang et al.

Summary: Mitochondria are intracellular energy generators whose dysfunction can lead to serious diseases. Understanding the molecular mechanisms underlying mitochondrial dysfunction is crucial for treating mitochondrial diseases. This review summarizes the key genetic processes, core genetic components, and genetic methods used to alleviate the adverse effects of mutations on mitochondrial physiology and functions.

PHARMACEUTICS (2021)

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Review Pharmacology & Pharmacy

Targeting Mitochondrial Oncometabolites: A New Approach to Overcome Drug Resistance in Cancer

Martina Godel et al.

Summary: Drug resistance is a major obstacle in successful cancer therapy, with mitochondria-derived oncometabolites playing a complex role in cancer biology, potentially leading to drug resistance. Oncometabolites can promote cancer aggressiveness and drug resistance through diverse pathways.

PHARMACEUTICS (2021)

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Review Pharmacology & Pharmacy

Mitochondrial Targeting Involving Cholesterol-Rich Lipid Rafts in the Mechanism of Action of the Antitumor Ether Lipid and Alkylphospholipid Analog Edelfosine

Faustino Mollinedo et al.

Summary: Edelfosine, an ether lipid, selectively induces apoptosis in tumor cells by interacting with cholesterol-rich lipid rafts, endoplasmic reticulum (ER), and mitochondria. Its mechanism involves recruitment of death receptors and ER stress signaling through lipid rafts in hematological cancer cells, and ER stress response in solid tumor cells. The involvement of lipid rafts and/or ER in edelfosine-induced apoptosis requires a mitochondrial-dependent step leading to cell death. Overexpression of Bcl-2 or Bcl-xL blocks this process. Additionally, edelfosine redistributes lipid rafts to mitochondria and recruits F1FO-ATP synthase into cholesterol-rich lipid rafts to induce cell death.

PHARMACEUTICS (2021)

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Review Pharmacology & Pharmacy