Necroptosis is cellular death that plays a significant role in several chronic diseases and viral infections. From septic shock to heart failure, stroke, and kidney failure – the understanding of necroptosis is critical in understanding these diseases. For example, necroptosis is involved in the loss of auditory nerve cells in multiple sclerosis. Researchers are attempting to understand necroptosis on a deeper level, as a better understanding of necroptosis allows for targeted research in potential therapeutic routes.
For a long time, necroptosis was a complete mystery to doctors and researchers. During the process of cellular death, the cell actually explodes – which baffled researchers for several years. We now know that cells activate pore-forming molecules that actually make holes in the membrane of the cell. This information allows for new perspectives in the treatment of both acute and chronic inflammatory and degenerative disease. If necroptosis can be blocked by specific drugs, this may allow circumvention in the resistance of malignant cells to chemotherapy, resensitizing these cells to cellular death and improving disease outcomes.
Some of the most common diseases involve inflammatory reactions resulting in cellular death. Understanding the process of cell death is essential for the development of effective treatment in these conditions. Current research focuses on new therapeutic strategies that may potentially counteract pore formation in necroptosis. The cellular explosion seen in cells during necroptosis is caused by the formation of pores that consist of something called MLKL proteins. Known as MLKL pores, these structures cause the cell to absorb too much water, causing cellular swelling and ultimately causing the cell to explode. A deeper understanding about MLKL proteins may lead to drugs that prevent or temporarily block this process – having significant effects on disease outcome.
Because inflammation plays a significant role in necroptosis, drugs and supplements that control systemic inflammation long-term may be useful for both prevention and treatment of conditions characterized by necroptosis. The use of non-steroid anti-inflammatory drugs (NSAIDs) in the fight against inflammation can be dangerous as a long-term treatment. NSAIDs can eat away at the lining of the stomach – placing consumers at risk for ulcers and gastrointestinal bleeding. For this reason, it’s a better idea to use nutritional therapy in controlling inflammation. The use of systemic enzymes is also a great alternative to NSAIDs. Systemic enzymes offer immune regulating benefits by naturally assisting the body in controlling and regulating inflammation.
Systemic enzymes like serrapeptase and nattokinase work within the blood stream by decreasing substances that are precursors to fibrin. Fibrin causes the blood to become thickened and can cause and contribute to a wide range of medical disorders. Fibrin can also accumulate within arterial walls and anywhere in the body that is plagued by chronic inflammation. Fibrin contributes to internal scarring and disease progression. The use of systemic enzymes on a long-term basis is also completely safe. Unlike NSAIDs, systemic enzymes pose no risk to the gastrointestinal lining or to organs like the kidneys and liver. The use of nutritional therapy combined with the regular use of systemic enzymes offers protection against necroptosis and inflammatory-related conditions without adverse side effects, and should be utilized prior to more invasive treatment routes.