Aged dermal white adipose tissue secretes monocyte chemoattractant protein-1 (MCP-1), which recruits macrophages to the area surrounding hair follicles and shifts the local inflammatory balance toward an M1-dominant state. In aged mice, depleting skin macrophages pushed follicles out of resting phase into active growth and restored pigmentation-related proteins, identifying the fat–chemokine–macrophage axis as a modifiable driver of age-related hair loss and graying.
Key Points
- Aged dermal fat secretes MCP-1, drawing macrophages to hair follicles
- Macrophage depletion restored follicle growth phase and pigmentation proteins
- M1 macrophages delayed growth; M0 and M2 accelerated it
Longevity Analysis
Hair loss and graying track with a broader aging pattern in which resident fat tissue becomes a signaling source for low-grade inflammation, redirecting immune cells toward tissue that depends on cyclical regeneration. The relevant variable is not follicle depletion but the chemical environment surrounding it — remove the inflammatory signal and the regenerative program resumes. Visible changes in hair offer an accessible external readout of immune and metabolic conditions in the skin, and interventions aimed at the inflammatory microenvironment rather than the follicle itself warrant closer attention.
Original published by Wiley Aging Cell, by Jian Chen, Yuhui Hou, Ke Ye, Yilong Guo, Pingping Sun, Fangfang Qi, Zhexiang Fan, Damao Dai, Xiaomin Liu, Shulian Wu, Demengjie Le, Zhiqi Hu, Yong Miao, Qian Qu .