Targeting Cellular Senescence In Diabetic Kidney Disease: Potential Of Regenerative, Cell-Based Therapies And Other Senotherapeutic Approaches

Aging Theory
Aging Pathway
Therapeutic
Cellular senescence, a state where cells stop dividing and accumulate, is a significant contributor to diabetic kidney disease, and new therapies are emerging to target these cells to improve kidney health.
Author

Gemini

Published

February 4, 2026

Our bodies are made of cells, and sometimes these cells enter a state called “senescence.” This means they stop dividing and can accumulate, releasing harmful substances that cause inflammation and damage to surrounding tissues. In conditions like diabetic kidney disease, this accumulation of senescent cells is a major problem, driving the progression of the disease and hindering the kidney’s ability to repair itself.

Fortunately, scientists are exploring exciting new ways to combat this. One approach involves “senotherapeutics,” which are treatments designed to specifically target these problematic senescent cells. These can be broadly categorized into two types: “senolytics,” which are like a clean-up crew that eliminates senescent cells, and “senomorphics,” which aim to change the harmful signals these cells send out.

Beyond senotherapeutics, regenerative medicine offers promising avenues. This includes “cell-based therapies,” where healthy cells, such as mesenchymal stem cells, or their beneficial secretions (extracellular vesicles) are used to help repair damaged kidney tissue. “Tissue engineering” is another innovative field that uses special materials like hydrogels to create structures that can support kidney regeneration.

Advanced technologies like gene editing (CRISPR) and specialized cell therapies (CAR-T) are also being investigated to precisely target and reduce the number of senescent cells and the inflammation they cause. The ultimate goal of these diverse strategies is to restore kidney function and prevent the progression of diabetic kidney disease by addressing the root cause of cellular aging and damage.


Source: link to paper