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Heat stress exacerbates metabolic dysfunction through skin-hypothalamus axis via KLK14 and astrocyte reprogramming

By

Jia-Jun Zhao3 Send email to [email protected]

6h ago· 83 min readenInsight

Summary

This research article investigates the link between heat stress and metabolic dysfunction. Using mouse models, the study reveals that exposure to heat stress increases susceptibility to diet-induced metabolic disorders. The mechanism involves a skin-hypothalamus axis where elevated skin-derived KLK14 (kallikrein-related peptidase 14) epigenetically reprograms hypothalamic LRRC7+ astrocytes, which in turn suppress neighboring paraventricular nucleus (PVN) OXT neurons. The study also demonstrates that Vitamin A can reduce KLK14 levels and mitigate metabolic impairment in both mice and humans, suggesting a potential therapeutic approach for heat-stress-related metabolic conditions.

Source

bskyHeat stress exacerbates metabolic dysfunction through skin-hypothalamus axis via KLK14 and astrocyte reprogrammingcell.com

Key quotes

· 3 pulled
We report that mice exposed to heat stress were more susceptible to metabolic dysfunction upon subsequent exposure to an obesogenic diet.
Heat stress activates a skin-hypothalamus axis via KLK14-dependent epigenetic reprogramming of LRRC7⁺ astrocytes, thereby exacerbating diet-induced metabolic dysfunction.
Vitamin A reduces KLK14 levels and mitigates metabolic impairment in both mice and humans.
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Heat stress activates a skin-hypothalamus axis via KLK14-dependent epigenetic reprogramming of LRRC7⁺ astrocytes, thereby exacerbating diet-induced metabolic dysfunction. Vitamin A reduces KLK14 levels and mitigates metabolic impairment in both mice and h

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