Psychosocial stress (PSS) is a significant contributor of inflammation and CVD.
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NLRP3 inflammasome activation amplifies inflammation in response to PSS.
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ER stress is a key upstream mechanism that triggers NLRP3 inflammasome activation.
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This study reveals mechanisms and targets to reduce inflammation caused by PSS.
Abstract
Psychosocial stress (PSS) affects all humans with different intensities and is known to significantly increase inflammation and cardiovascular disease [1,2]. An amplifier of inflammation is an intracellular multiprotein complex, the inflammasome, activation of which leads to pro-inflammatory cytokines production. However, the mechanisms leading to the inflammasome activation in the heart by PSS are not well understood. Here, we identify critical upstream mechanisms leading to NLRP3 inflammasome activation via endoplasmic reticulum (ER) stress and JAK/STAT pathway. These findings reveal important mechanistic insights into possible upstream targets in controlling excessive inflammation due to PSS.
https://www.jmcc-online.com/article/S0022-2828(25)00119-1/abstract
2 Medical News 