Key Findings

Adaptive Tissue Remodeling

Aging impairs progenitor-dependent beige adipocyte recruitment. Our studies demonstrated that aging limits the ability of adipose tissue to generate thermogenic beige adipocytes, revealing a fundamental decline in adaptive tissue remodeling.

Representative publication

Reversing Pdgfrβ signaling restores metabolically active beige adipocytes by alleviating ILC2 suppression in aged and obese mice.
Age-dependent Pdgfrβ signaling drives adipocyte progenitor dysfunction to alter the beige adipogenic niche in male mice.
Cellular Aging Contributes to Failure of Cold-Induced Beige Adipocyte Formation in Old Mice and Humans.

 
 

Neurovascular Control of Thermogenesis

Macrophages maintain tissue networks required for thermogenic function. We discovered that macrophages support neurovascular organization within brown adipose tissue and are required for proper thermogenic responses.

Representative publication

Smooth muscle cell-derived Cxcl12 directs macrophage accrual and sympathetic innervation to control thermogenic adipose tissue.
Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure.
Remodeling of gene regulatory networks underlying thermogenic stimuli-induced adipose beiging.

 

Developmental Regulation of Muscle Adaptation

Our work identified a developmental checkpoint regulating muscle adaptation and regenerative capacity. For instance, we have identified PDGFRβ signaling as a regulator of skeletal muscle growth and regeneration.

Representative publication

PDGFRβ signaling restrains myocyte function to limit the regenerative capacity of skeletal muscle.
Pyruvate Kinase M2 Supports Muscle Progenitor Cell Proliferation but Is Dispensable for Skeletal Muscle Regeneration after Injury.