Pausing cell death, known as necrosis, may be the secret to defying the aging process

Aging has long been viewed as a slow and inevitable decline. But new research suggests that hidden deep within the body’s cellular processes, there may be a crucial trigger point – one that could be changed, paused, or even reversed. The process in question is necrosis, a form of uncontrolled cell death.

A study by researchers from University College London (UCL), LinkGevity, and the European Space Agency (ESA) places necrosis at the center of aging and disease. The paper suggests that necrosis might not just be a consequence of damage. It might be a cause.

Necrosis may be the trigger of aging

Necrosis is a chaotic form of cell death caused by stress, infection, or injury. Unlike controlled cell death, it damages nearby tissues and triggers inflammation. The study suggests necrosis is not just a final event but an active driver of aging and chronic disease.

“Nobody really likes talking about death, even cell death, which is perhaps why the physiology of death is so poorly understood. And in a way necrosis is death,” noted Dr. Keith Siew from the UCL Centre for Kidney & Bladder Health.

“If enough cells die, then tissues die, then we die. The question is what would happen if we could pause or stop necrosis.”

Chaotic cell death spreads damage

Cells are the building blocks of all living organisms. Their death is natural and necessary, but only when it happens in a regulated way.

In healthy systems, cells are replaced in a clean and controlled fashion. This process, known as apoptosis, helps organs regenerate and stay functional.

Necrosis is different. It happens without order or purpose. When it occurs, cells rupture and spill their contents into surrounding tissue. This creates inflammation, spreads damage, and accelerates aging.

“Necrosis remains one of the last frontiers in medicine – a common thread across aging, disease, space biology, and scientific progress itself,” said Dr. Carina Kern, lead author of the study and CEO of LinkGevity.

Calcium imbalance causes cell collapse

At the heart of necrosis is calcium, a mineral that helps regulate cell function. Normally, cells maintain much higher calcium levels outside their membranes than inside. This gradient helps control vital activities.

When calcium floods in, the cell collapses, spills toxins, and triggers harmful inflammation. “When cells die, it’s not always a peaceful process for the neighbors,” Dr. Siew noted.

Toxic cell death links diseases

Necrosis triggers a domino effect. As toxic materials spread, nearby cells are affected. This leads to more cell death, more inflammation, and a growing spiral of decline. Over time, the body becomes less able to repair itself.

The study draws connections between necrosis and several chronic conditions. These include Alzheimer’s, heart disease, and kidney failure. These diseases are often seen as unrelated, but researchers argue they share a common thread: necrosis.

“Necrosis has been hiding in plain sight. As a final stage of cell death, it’s been largely overlooked. But mounting evidence shows it’s far more than an endpoint. It’s a central mechanism through which systemic degeneration not only arises but also spreads,” noted Dr. Kern.

“That makes it a critical point of convergence across many diseases. If we can target necrosis, we could unlock entirely new ways to treat conditions ranging from kidney failure to cardiac disease, neuro-degeneration, and even aging itself.”

Cell death harms kidneys as we age

Among all the organs affected by necrosis, the kidneys may suffer the most. They filter blood, regulate fluid levels, and support other systems. As people age, these functions often falter. Nearly half of those over 75 show signs of kidney disease.

The study highlights how necrosis lies at the center of this decline. Stressors such as low oxygen, oxidative stress, and toxin buildup all lead to necrosis in kidney tissues. Once it begins, it fuels a feedback loop that becomes hard to stop.

“With kidney disease, there’s no one underlying reason that the kidneys fail. It could be a lack of oxygen, inflammation, oxidative stress, a build-up of toxins, and so on,” Dr. Siew explained

“All of these stressors eventually lead to necrosis, which initiates a positive feedback loop that spirals out of control, leading to kidney failure. We can’t stop all of these stressors, but if you could intervene at the point of necrosis, you’d effectively achieve the same result.”

Aging in space

The implications of necrosis extend far beyond Earth. In space, astronauts face conditions that mimic and accelerate aging. Low gravity and cosmic radiation stress the body. Muscles waste away, bones weaken, and organs begin to fail more quickly than on Earth.

In 2024, Dr. Siew worked on a study that identified the human kidney as a major vulnerability during spaceflight. Necrosis appeared to play a central role. The body’s inability to manage stress in space could threaten the success of long-term missions.

Damian Bailey is a professor of physiology and biochemistry at the University of South Wales and Chair of the ESA Life Sciences Working Group.

“Targeting necrosis offers potential to not only transform longevity on Earth but also push the frontiers of space exploration,” noted Professor Bailey. “In space, the same factors that cause aging on Earth are made worse by cosmic radiation and microgravity – speeding up degeneration dramatically.”

Stopping cell death to support healing

Necrosis in vital organs triggers damage cycles that slow healing and reduce recovery capacity.

“In many age-related diseases – affecting diverse organs such as the lungs, kidneys, liver, brain, and cardiovascular system – relentless cascades of necrosis fuel the progression of disease,” explained Dr. Kern.

“This is often alongside impaired healing that leads to fibrosis, inflammation and damaged cells. Each cascade triggers and amplifies the next.”

“If we could prevent necrosis, even temporarily, we would be shutting down these destructive cycles at their source, enabling normal physiological processes and cell division to resume – and potentially even allowing for regeneration.”

The study is published in the journal Oncogene.

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