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Psychosocial stress amplifies inflammation through NLRP3 Inflammasome activated by endoplasmic reticulum stress in the mouse heart

  • Daphne Diloretto
  • , Gaurav Sarode
  • , Phung N. Thai
  • , Jeong Han Lee
  • , Evelyn Navar
  • , Jeong eun Park
  • , Chaitali Khadilkar
  • , Ning Zong
  • , Yu Jia Dong
  • , Avni Duda
  • , Erick Romero
  • , Pablo E. Acevedo
  • , Xiao Dong Zhang
  • , David A. Liem
  • , Imo Ebong
  • , Javier E. Lopez
  • , Heejung Bang
  • , Chao Yin Chen
  • , Leighton Izu
  • , Martin Cadeiras
  • Ebenezer N. Yamoah, Nipavan Chiamvimonvat, Padmini Sirish

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)39-43
Number of pages5
JournalJournal of Molecular and Cellular Cardiology
Volume206
DOIs
StatePublished - Sep 2025

Keywords

  • ER stress
  • Inflammasome
  • Inflammation
  • Oxylipins

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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