Mitochondria are the energy factories of the cell, and the focus of Mytohealth. These organelles extract nutrients from cells and convert them into ATP, energy currency used by every cell and tissue in the body.
Mitochondria are factories of energy that generate ATP and sustain life. Less is known about their role as a signaling apparatus that promote health and induce cell death when necessary.
Due to high metabolic demand, neurons and especially dopaminergic regions of the brain are especially susceptible to mitochondrial damage. Maintaining mitochondrial homoeostasis is central to cellular survival.
While the Y chromosome is passed on from father to son, a mother’s Mitochondria is inherited by both sexes. This unique genetic inheritance plays a profound role in metabolic lineage and disease vulnerability.
Disruption in mitochondrial energy output is a root driver of Alzheimer’s disease and Parkinson’s disease, impairing synaptic signaling and neuronal survival.
Progressive mitochondrial decline leads to degradation in muscle movement, memory, and cognition across age-related pathways.
Mitochondrial defects compromise cardiometabolic systems, vascular recovery from ischemic stress, and cellular regulation linked to cancer.
While mitochondria are prone to damage through mutations, ischemia, environment, oxidative stress, and other hazards, they are quickly repaired by a process called “mitophagy”.
Damage to mitochondria leads to loss of energy, accumulation of misfolded proteins and aggregates that in turn de-polarize mitochondria, causing further loss of ATP and ultimately cell death.
The UPS is responsible for the removal of damaged mitochondria (mitophagy) and also plays a fundamental role in development of new mitochondria, or “mitobiogenesis”.
Figure: Neuronal mitochondrial cascade — Complex I deficiency, bioenergetic failure, and quality control regulators (Parkin, PINK1, α-syn).
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