College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing 163319, Heilongjiang Bayi, China.
J Vet Sci. 2023 Jan;24(1):e2. doi: 10.4142/jvs.22185.
Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear.
This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms.
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.
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 stress-involved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia.
These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.
低温是一种重要的环境因素，会增加心血管疾病的风险，但其中的作用机制尚不清楚。
本研究旨在探讨冷应激（CS）在心肌损伤中的作用及其潜在机制。
本研究构建了慢性 CS 诱导的心肌损伤模型；小鼠每天在 4°C 下接受 3 小时的慢性 CS 处理，持续 3 周。
CS 可通过诱导热休克蛋白 70（HSP70）水平升高、肌酸磷酸激酶同工酶（CKMB）和丙二醛（MDA）生成增加、肿瘤坏死因子-α（TNF-α）、高迁移率族蛋白 B1（HMGB1）、白细胞介素 1β（IL-1β）、白细胞介素 18（IL-18）和白细胞介素 6（IL-6）含量增加，导致心肌损伤，并耗竭超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽（GSH）。冷暴露激活了多种信号通路，包括与细胞焦亡相关的 NOD 样受体 3（NLRP3）调控的半胱氨酸天冬氨酸蛋白酶 1（caspase-1）依赖性/天冬氨酸半胱氨酸酶 1（GSDMD）、炎症相关的 Toll 样受体 4（TLR4）/髓样分化因子 88（MyD88）介导的核因子 kappa B（NF-κB）、丝裂原活化蛋白激酶（MAPK）以及涉及硫氧还蛋白 1/硫氧还蛋白相互作用蛋白（Txnip）信号通路的氧化应激，这些通路在低温引起的心肌损伤中发挥关键作用。
这些发现为极低温度下心血管疾病风险增加提供了新的见解。
