Mitochondria

Mitochondria are double-membraned organelles inside almost every human cell, and their main job is to convert fuel and oxygen into ATP, the molecule that pays for nearly all cellular work. They also decide when a cell dies, buffer calcium, generate heat, and — unusually — carry a small genome of their own, inherited only from the mother.

What they are

A mitochondrion has an outer membrane, an inner membrane folded into cristae, and a central matrix. The folding matters: the inner membrane holds the electron transport chain, and more surface area means more capacity. Cells with high energy demand — heart, skeletal muscle, brain — carry the most.

Their own DNA (mtDNA) encodes 37 genes, including 13 proteins of the respiratory chain. The remaining roughly 1,500 mitochondrial proteins are encoded in the nucleus and imported. Because mtDNA sits close to the site of electron leakage and has limited repair machinery, it accumulates mutations faster than nuclear DNA.

What they do

ATP production. Fuel breakdown reduces NAD+ to NADH. NADH hands its electrons to the transport chain, which pumps protons across the inner membrane. The proton gradient then drives ATP synthase, in the process called oxidative phosphorylation.

Apoptosis. Mitochondria release cytochrome c to trigger programmed cell death — the controlled removal of damaged cells.

Calcium handling and heat. They store calcium for signalling, and in brown fat they deliberately short-circuit the proton gradient to produce heat instead of ATP.

Quality control. Damaged mitochondria are recycled by mitophagy, and new ones are built by biogenesis under PGC-1α control. Exercise and fasting both push this balance towards renewal.

Mitochondria and ageing

Mitochondrial function declines with age: fewer and less efficient organelles, more mtDNA damage, more electron leakage. Whether that decline is a cause of ageing or a consequence of it remains contested — but it is measurable, and it is the rationale behind most “cellular energy” compounds.

Why peptides care

• MOTS-c is remarkable for being encoded inside mitochondrial DNA rather than in the nucleus. Under metabolic stress it moves to the cell nucleus and helps direct a metabolic and antioxidant response, partly through AMPK activation.
• NAD+ supplies the coenzyme the electron transport chain depends on; restoring it is the stated aim of NR and NMN supplementation.

Related concepts

The electron leakage that makes mitochondria a source of reactive oxygen species is covered in oxidative stress; the coenzyme that feeds them has its own article at NAD+.