Key result
Aging in human subcutaneous adipose tissue shifts the intercellular microenvironment to be dominated by inflammatory M1 macrophages, resulting in the accumulation of dysfunctional PLAU+ adipose progenitor cells.
Why the study?
Age-dependent adipose tissue malfunction increases disease risk, but little is known about the cellular and molecular basis of human adipose tissue aging.
Senescent M1 macrophages drive adipose progenitor cell aging through chemokine signaling, identifying PLAU+ adipose progenitor cells as a potential therapeutic target for aging-related adipose tissue dysfunction.
May support adipose tissue-targeted therapies in age-related cardiometabolic disease; leaves open need for human validation and trials.
Age-dependent adipose tissue malfunction raises the risk of diseases like diabetes, cardiovascular disease, and even cancer by contributing to metabolic decline, heterotopic fat storage, and chronic systemic inflammation. 1 Understanding adipose tissue aging requires in-depth knowledge of the cellular and molecular properties of various adipose tissue cell types. Although the heterogeneity of the cell population during mouse aging has been studied, 2 little is known about the cellular and molecular basis of human adipose tissues aging.
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Zhou et al. (2023) conducted a letter in Adipose tissue aging (n=14). Aging vs. Young age was evaluated on Accumulation of PLAU+ inflammatory adipose progenitor cells (APC5). Aging in human subcutaneous adipose tissue shifts the intercellular microenvironment to be dominated by inflammatory M1 macrophages, resulting in the accumulation of dysfunctional PLAU+ adipose progenitor cells.
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