Autophagy-Senescence Interplay In Kidney Disease: Mechanistic Insights And Therapeutic Potential
Have you ever thought about how your cells keep themselves clean and healthy? Our bodies have incredible mechanisms, and two crucial ones are cellular “self-eating,” known as autophagy, and cellular aging, or senescence. Autophagy is like a cellular recycling program, where cells break down and remove damaged parts, misfolded proteins, and waste. This process is vital for maintaining energy balance and keeping cells young and functional.
However, as we age or face constant stress, this self-cleaning process can slow down. When that happens, old, damaged cells, which we call senescent cells or “zombie cells,” start to accumulate. These senescent cells don’t just sit there; they actively release harmful inflammatory chemicals and factors that promote scarring.
In a hardworking organ like the kidney, this imbalance between efficient self-cleaning and the buildup of aging cells can lead to serious problems. It significantly contributes to the development and progression of chronic kidney disease (CKD) and acute kidney injury (AKI). The interaction between reduced autophagy and increased senescent cells worsens kidney damage, causing issues like the shrinking of kidney tubules and scarring in the filtering units.
The good news is that understanding this intricate cellular dance opens up exciting new possibilities for treatment. Researchers are exploring therapies aimed at boosting the cell’s self-cleaning ability, eliminating those harmful “zombie cells,” or using protective substances like antioxidants and stem cells. While there are still challenges, such as ensuring these treatments target only the necessary cells, focusing on this interplay between cellular self-cleaning and aging holds great promise for developing more precise and effective ways to combat kidney diseases.
Source: link to paper