Mitochondria are often introduced in textbooks as the “powerhouses of the cell,” tiny bean-shaped organelles quietly generating the energy that keeps us alive. But the truth is far stranger and far more dynamic. Mitochondria aren’t isolated little beans floating around — they’re an ever-shifting network, constantly undergoing fusion and fission events. Sometimes they merge into vast webs snaking through the cell like cobwebs; other times, they split apart to work independently.
What’s more, mitochondria are the only part of the cell, apart from the nucleus, that contain their own DNA — circular mini-genomes tucked within each organelle. A single mitochondrion can house up to ten copies of this DNA, a molecular inheritance from their ancient bacterial ancestors.
Ageing and the Fading Fire of the Mitochondria
As we grow older, our mitochondria begin to falter. They become fewer in number and less efficient at producing energy. Scientists often use the amount of mitochondrial DNA in a person’s cells as a rough measure of mitochondrial abundance — and the findings are sobering. People with the least mitochondrial DNA are not only weaker and frailer but also up to 50 percent more likely to die than those with the richest mitochondrial reserves.
Mutations in mitochondrial DNA also accumulate with age, mirroring what happens to nuclear DNA. Meanwhile, a specialized cleanup process called mitophagy — which selectively removes malfunctioning mitochondria — gradually declines. As damaged mitochondria pile up, the cell’s energy grid starts to flicker and fail.
The Mitochondrial Link to Age-Related Disease
Mitochondria are most critical in energy-demanding tissues like muscle and brain. In muscles, mitochondrial damage contributes to the loss of strength and mass that comes with age. In the brain, where only 2 percent of body weight consumes a staggering 20 percent of the body’s energy, mitochondrial malfunction has been implicated in neurodegenerative diseases like Parkinson’s and Alzheimer’s.
Decades ago, biologists proposed the mitochondrial free radical theory of ageing. Mitochondria, by producing energy, generate highly reactive molecules — especially oxygen radicals — that can damage proteins and DNA. Free radicals like OH, NO, and ONOO are biological troublemakers capable of causing widespread molecular chaos.
Free Radicals: Villains or Messengers?
For years, scientists imagined that if we could just neutralize these free radicals, we could slow ageing. Yet experiments have overturned this simple narrative. Mice bred with extra anti–free radical genes live no longer than normal, and even worms completely stripped of their free-radical defenses suffer cellular damage but age at the same rate.
It turns out that free radicals aren’t just destructive. They’re also vital messengers. Cells use them to signal growth, halt division, or trigger self-destruction when something goes wrong. Immune cells even weaponize them to wipe out bacteria. Far from being mere biochemical berserkers, free radicals are now seen as players in a complex molecular conversation — just another sign of evolution’s deep negotiation with chaos.
Still, their double-edged nature means they remain central to ageing. Mitochondria, as both the main source and target of free radicals, are deeply entangled in the cell’s life-and-death decisions.
Inflammation and the Fire Within
Another biological process intertwined with ageing is inflammation. When the immune system detects infection or injury, it releases molecules that summon reinforcements — a protective swelling that helps the body heal. In youth, this system works beautifully. But over time, the inflammatory response can get stuck in “always-on” mode.
This slow, simmering state is called chronic inflammation, or more evocatively, inflammageing. Blood tests can detect it: levels of C-reactive protein and interleukin-6 rise steadily with age. People who show high levels of these markers face greater risks of cancer, heart disease, dementia, and other age-related conditions.
Part of the problem comes from senescent cells — old cells that refuse to die and instead release inflammatory signals known as SASP (senescence-associated secretory phenotype). Add to that the accumulation of damaged proteins, persistent low-grade infections, and a tired immune system, and the body becomes a battlefield of constant low-level alarm.
A Burning Link: Inflammation and Metabolic Disease
Even diseases like diabetes are part of this larger inflammatory web. It’s not just an excess of sugar that drives insulin resistance — inflammation does too. Acute infections can cause insulin levels to spiral as the body’s immune defenses go into overdrive. Ageing produces a slower, subtler version of that same process, as inflammation gradually undermines the body’s ability to manage blood sugar.
Mitochondria and inflammation, then, are two sides of the same story: the fading energy of our cells and the overzealous defense of our immune system. Both evolved to protect life — yet both, when pushed too far or left unchecked, contribute to the gradual unraveling we call ageing. Understanding them not as villains but as parts of a complex biological balance may be the first step toward ageing with resilience and grace.
Source : Ageless: The New Science of Getting Older Without Getting Old by Andrew Steele
Goodreads : https://www.goodreads.com/book/show/52954648-ageless
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