Researchers at WashU Medicine have identified a new cellular process called cathartocytosis. When cells are injured, they can expel parts of their internal machinery, shedding damaged components. This reset allows them to revert to a more primitive, stem cell–like state, which increases their capacity to repair and regenerate tissue.
- It’s been well established that cells can remove damaged parts through mechanisms like autophagy (self-digestion) or apoptosis (programmed cell death).
- But cathartocytosis is different: instead of digesting components internally or dying, the cell expels its damaged internal machinery outward, almost like throwing out broken parts, and then “resets” itself.
- This allows the cell to revert to a stem-like state and begin repairing tissue, which is something not seen in other well-studied processes.
“After an injury, the cell’s job is to repair that injury. But the cell’s mature machinery for doing its normal job gets in the way. So, this cellular cleanse is a quick way of getting rid of that machinery so it can rapidly become a small, primitive cell capable of proliferating and repairing the injury. We identified this process in the GI tract, but we suspect it is relevant in other tissues as well.”
— Jeffrey W. Brown, MD, PhD, assistant professor of medicine in the Division of Gastroenterology at WashU Medicine and first author of the study
This is a strategic shortcut. When they expel their specialized structures, cells effectively reset themselves. For tissues like the stomach lining, where quick recovery is essential, this is a useful mechanism.
But the catch is that this process is messy. The expelled debris can linger and spark inflammation and even feed cancer development. Persistent or excessive cathartocytosis, (especially in the context of chronic injury) may fuel inflammatory states, make chronic injuries harder to resolve, and create a cancerous environment.
While more research is needed, the study authors suspect that cathartocytosis could play a role in promoting injury and inflammation in Helicobacter pylori infections in the gut.
H. pylori is a type of bacteria known to infect and damage the stomach, causing ulcers and increasing the risk of stomach cancer. With more information about this process, we should be able to develop ways to encourage a proper healing response and block the process of cathartocytosis when an injury does happen.
I have a few theories about what could cause this rapid healing process, and what we can do to encourage proper healing.
Stress-induced organelle expulsion seems tied to failing energy systems: for instance, mitochondrial expulsion increases during autophagy deficiency or mitochondrial damage, both of which compromise cellular energy production.
A cell resorts to cathartocytosis when its energy balance is critically impaired. In other words, if mitochondria can’t produce enough ATP to repair damage internally, the cell takes a shortcut: it expels its complex structures so it can regress to a simpler, lower-energy state.
Organelle release, whether lipids, mitochondria, or protein fragments, can serve as fuel or signaling molecules for nearby tumor cells, especially if energy production is disrupted in the local cells.
Scientific Evidence for this Theory:
- Neurons and PC12 cells under chemical stress (CCCP or rotenone) were observed to release depolarized mitochondria into the extracellular space. This release increased when autophagy pathways were impaired, indicating a route of last resort when intracellular cleanup fails.
- Exophers in C. elegans are membrane-bound vesicles containing mitochondria and other cellular components. Their production is triggered by stressors, mitochondrial damage, or impaired autophagy.
- In cardiac tissue, under baseline conditions or stress, cardiomyocytes eject exophers loaded with damaged mitochondria, which neighboring macrophages phagocytize. This “heterophagy” helps manage cell stress and preserve heart health.
If cathartocytosis is a desperate measure cells use when energy is low and healing is needed, then the best way to prevent this pathological cycle is to optimize energy metabolism and reduce chronic injury signals.
Here are a few practical steps:
- Support mitochondrial energy production
- Prioritize nutrient-dense foods: easily digested proteins (eggs, dairy, gelatin, seafood), ripe fruits, and roots.
- Adequate B-vitamins (especially niacinamide, thiamine, and riboflavin) are essential for efficient ATP production.
- Reduce chronic stressors
- Manage cortisol through regular meals, rest, and muscle-building exercise.
- Limit exposure to toxins (seed oils, endocrine disruptors, glyphosate) that damage mitochondria.
- Promote cellular clean-up without excess debris
- Adequate thyroid function supports orderly repair rather than chaotic breakdown.