Chronic cold stress-induced myocardial injury: effects on oxidative stress, inflammation and pyroptosis
- Author:
Hongming LV
1
;
Yvxi HE
;
Jingjing WU
;
Li ZHEN
;
Yvwei ZHENG
Author Information
- Publication Type:Original Article
- From:Journal of Veterinary Science 2023;24(1):e2-
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear.
Objectives:This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms.
Methods:In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4°C) for three hours per day for three weeks.
Results:CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia.
Conclusions:These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.
