Shear Stress Governs Hematopoietic Stem Cell Fate To Promote Inflammation-Induced Aging

Aging Theory
Aging Pathway
Therapeutic
Blood flow forces, known as shear stress, activate a protein called PIEZO1 in blood-forming stem cells, leading to their increased proliferation and a shift towards producing more immune cells, thereby accelerating inflammation-driven aging.
Author

Gemini

Published

January 14, 2026

Our bodies contain special cells called hematopoietic stem cells (HSCs) that live in the bone marrow and are responsible for producing all types of blood cells. Normally, these stem cells are quiet, but they can be called into action by things like inflammation or stress. As we age, and especially with chronic inflammation, these stem cells can start to age faster themselves, leading to an imbalance where they produce too many immune cells and fewer of other important blood cells. This imbalance contributes to the overall aging process.

Recent research has uncovered a fascinating link between the physical forces of blood flow and the aging of these crucial stem cells. It turns out that a protein called PIEZO1, which acts as a mechanical sensor, plays a key role. When blood flows, it creates a “shear stress” on the cells. PIEZO1 senses this force, triggering a cascade of events within the HSCs. This activation causes the stem cells to multiply more rapidly and to preferentially produce certain types of immune cells, a process known as myelopoiesis. This accelerated activity, driven by mechanical forces, ultimately contributes to the inflammation-induced aging of the stem cells.

Importantly, scientists found that by blocking PIEZO1 with a specific compound, they could reduce this accelerated aging in mice. This discovery highlights a previously unrecognized mechanism by which physical forces in our blood vessels influence the aging of our stem cells and, consequently, our overall health. Understanding this pathway could open new avenues for therapies aimed at combating age-related diseases and promoting healthier aging.


Source: link to paper