How You Can Harness Mitophagy and Autophagy to Fight Age-Related Disease

A recent article published in Medriva provides an overview of autophagy and mitophagy, crucial cellular processes involved in the degradation and recycling of dysfunctional or unnecessary cellular components. Many healthcare providers need to pay more attention to this topic. Specifically, mitophagy is cargo-specific autophagy responsible for the selective removal of damaged or dysfunctional mitochondria.

The article highlights the importance of mitophagy in maintaining cellular homeostasis and preventing the accumulation of potentially harmful materials. It also discusses the pathways involved in mitophagy, such as the PINK1 and parkin proteins, and how defects in these pathways have been linked to neurodegenerative diseases like Parkinson’s. Additionally, the article explores the evolutionary origin of mitophagy and the role of autophagy-related genes (ATGs) in mediating this process. It also touches on the potential therapeutic value of targeting mitophagy and mitochondrial biogenesis in treating diseases related to mitochondrial dysfunction.

Understanding autophagy and mitophagy in regenerative medicine is significant because they can address cellular dysfunction and promote tissue regeneration. Mitophagy is crucial in maintaining healthy mitochondria, essential for cellular energy production and overall cellular function. 

By selectively removing damaged mitochondria, mitophagy can prevent the accumulation of dysfunctional organelles and facilitate the regeneration of healthy cells and tissues.

In regenerative medicine, modulating mitophagy and autophagy could enhance the efficacy of stem cell therapies, tissue engineering approaches, and other regenerative strategies. Promoting the clearance of damaged cellular components and maintaining mitochondrial health could improve the survival, proliferation, and differentiation of stem cells or progenitor cells used for tissue regeneration. Furthermore, targeting mitophagy and autophagy pathways could address age-related cellular dysfunction and promote tissue rejuvenation. 

As cells age, they accumulate damaged organelles and protein aggregates, contributing to cellular dysfunction and age-related diseases. By enhancing mitophagy and autophagy, it may be possible to remove these damaging factors and restore cellular function, potentially slowing or reversing certain aspects of aging. This is a subject that requires our attention. It certainly has mine.

Increase Autophagy and Mitophagy with EBO2 and more…

A straightforward way to increase these cellular processes is to practice intermittent fasting. This is a potent stimulator of these modalities. Some supplements that may be beneficial include Urolithin A and Spermidine. 

We also have several modalities that will stimulate autophagy and mitophagy. These include EBO2, hyperbaric oxygen, and intermittent hypoxia. These modalities work in similar fashions.

EBO2 is a potent stimulator of the NRF2 (nuclear factor erythroid 2-related factor 2) pathway that can induce both mitophagy and autophagy. NRF2 activation is a protective mechanism against oxidative stress, mitochondrial dysfunction, and the accumulation of damaged proteins or organelles by upregulating the expression of critical genes involved in mitophagy and autophagy. This process helps maintain cellular homeostasis and prevent the onset of various diseases associated with oxidative stress and proteotoxicity.

NRF2 is a transcription factor that regulates the expression of various genes involved in the cellular antioxidant response and maintains homeostasis. The relationship between NRF2 and mitophagy (selective degradation of damaged mitochondria) is as follows: 

Oxidative stress or mitochondrial dysfunction can activate NRF2, which then translocates into the nucleus. NRF2 upregulates the expression of several genes involved in mitophagy, such as PINK1 (PTEN-induced putative kinase 1), PARKIN (an E3 ubiquitin ligase), and p62 (an adaptor protein). These proteins coordinate the recognition, labeling, and selective removal of damaged mitochondria through the autophagy pathway.

Similarly, NRF2 can also stimulate general autophagy (bulk degradation of cytoplasmic components) through various other mechanisms. 

This is an exciting article highlighting how we can harness many of PUR-FORM’s modalities to increase the autophagy and mitophagy processes in our own bodies!

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Joseph Purita, MD