MAS Receptor Agonists for Stimulating Mitochondrial Turnover
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Solution Overview
Problem
Mitochondrial dysfunction is associated with various serious medical disorders, and existing treatments are inadequate for stimulating mitochondrial turnover to address these conditions.
Innovation Solution
Administering MAS receptor agonists or substances that trigger endogenous production of MAS receptor agonists to stimulate mitophagy, promoting mitochondrial turnover through mechanisms such as mTORC1 activation, NRF2 activation, and mitochondrial dynamics, thereby enhancing mitochondrial biogenesis and degradation.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If conventional treatments are used for mitochondrial dysfunction, then existing disease symptoms are addressed, but mitochondrial turnover remains insufficient to effectively treat diseases
Solution Approach 1:
The patent changes the physiological parameter of mitochondrial turnover by administering MAS receptor agonists that specifically stimulate mitophagy and mitochondrial biogenesis, transforming the static state of insufficient turnover into a dynamic state of enhanced mitochondrial replacement and renewal
Solution Approach 2:
The patent introduces MAS receptor agonists as intermediary substances that mediate between the administered compound and the mitochondrial turnover process, activating the MAS receptor to trigger downstream signaling pathways that enhance mitophagy and mitochondrial biogenesis
2Reliability
If mitochondrial turnover is stimulated to treat diseases, then disease symptoms are improved, but the complexity of treatment mechanisms increases
Solution Approach 1:
The patent segments the complex mitochondrial turnover process into distinct actionable pathways: mitophagy stimulation through MAS receptor activation, mTORC1 pathway modulation, and NRF2 pathway activation, allowing targeted intervention at specific points in the mechanism
Solution Approach 2:
The patent employs MAS receptor agonists that serve multiple functions simultaneously: activating the MAS receptor, stimulating mitophagy, enhancing mitochondrial biogenesis, and modulating antioxidant responses through NRF2, thereby addressing multiple aspects of mitochondrial dysfunction with a single therapeutic approach
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
Stimulating mitochondrial turnover effectively treats diseases associated with below-normal turnover, including inflammatory, neurodegenerative, and ocular diseases, by improving cellular energy production and reducing disease symptoms.
Implementation Method 1
MAS agonists target mitophagy pathways and can promote mitophagy via several mechanisms (such as mTORC1; NRF2 activation; TFEB expression; inhibition of ATP hydrolysis by mitochondrial Complex V; mitochondrial dynamics)
Implementation Method 2
MAS agonists target mitophagy pathways and can promote mitophagy via several mechanisms (such as mTORC1; NRF2 activation; TFEB expression; inhibition of ATP hydrolysis by mitochondrial Complex V; mitochondrial dynamics)
Implementation Method 3
MAS agonists target mitophagy pathways and can promote mitophagy via several mechanisms (such as mTORC1; NRF2 activation; TFEB expression; inhibition of ATP hydrolysis by mitochondrial Complex V; mitochondrial dynamics)
Implementation Method 4
Aerobic eukaryotes require mitochondria to produce most of their cells' adenosine triphosphate (ATP), the principal medium of intracellular chemical energy transfer, via oxidative phosphorylation (OXPHOS)
Data Source
AI summary
Provided herein are methods of stimulating mitophagy in a subject in need thereof administering to the subject a mitophagy-stimulating amount of a MAS receptor agonist or substance that triggers endogenous production of a MAS receptor agonist. The present disclosure also relates to medical intervention methods and agents, namely methods and agents for stimulation of mitochondrial turnover for treatment of disease in a mammal. The disclosure comprises a method of stimulating increased mitochondrial turnover in a mammal comprising administering to the mammal a pharmacologically suitable dose of a MAS receptor agonist; MAS receptor modulator; a substance that triggers endogenous production of a MAS receptor agonist; a substance that triggers endogenous production of a MAS receptor modulator; or any combination thereof. The pharmacological activity acting on MAS receptor in turn stimulates an increase in mitochondrial turnover in host cells, alleviating a disease state in the host mammalian organism.


