Jaswal Priya, Bansal Seema, Chaudhary Rishabh, Basu Jhilli, Bansal Nitin, Kumar Subodh
Department of Pharmacology, M.M. College of Pharmacy, Maharishi Markandeshwar (Deemed to be University), Mullana, Ambala, Haryana, 133207, India.
Department of Pharmacology, Institute of Medical Sciences Krishnanagar, Naida, West Bengal, India.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Mar;398(3):2535-2546. doi: 10.1007/s00210-024-03556-z. Epub 2024 Oct 28.
As climate change intensifies, urgent action is needed to address global warming and its associated health risks, particularly in vulnerable regions. Rising global temperature and increasing frequency of heatwaves present a hidden health risk, disrupting the body's temperature regulation and leading to severe consequences such as heat stress-induced multiple organ dysfunction (HS-MOD). Multiple organ injury triggered by heat stress involves complex molecular pathways such as nitric oxide dysregulation, inflammation, oxidative stress, mitochondrial dysfunction, calcium homeostasis disruption, and autophagy impairment that contribute to cellular damage. Understanding these molecular pathways is crucial for developing targeted therapeutic interventions to alleviate the impact of heat stress (HS). As we explore numerous therapeutic strategies, a remarkable molecule captures our attention: nitric oxide (NO). This colorless gas, mainly produced by nitric oxide synthase (NOS) enzymes, plays crucial roles in various body functions. From promoting vasodilation and neurotransmission to regulating the immune response, platelet function, cell signaling, and reproductive health, NO stands out for its versatility. Exploring it as a promising treatment for heat stress-induced multiple organ injury highlights its distinctive features in the journey towards effective therapeutic interventions. This involves exploring both pharmacological avenues, considering the use of NO donors and antioxidants, and non-pharmacological strategies, such as adopting nitrate-rich diets and engaging in exercise regimens. This review highlights the concept of heat stress, the molecular framework of the disease, and treatment options based upon some new interventions.
随着气候变化加剧,需要采取紧急行动应对全球变暖及其相关的健康风险,尤其是在脆弱地区。全球气温上升和热浪频率增加带来了隐藏的健康风险,扰乱人体的体温调节,导致诸如热应激诱导的多器官功能障碍(HS-MOD)等严重后果。热应激引发的多器官损伤涉及复杂的分子途径,如一氧化氮失调、炎症、氧化应激、线粒体功能障碍、钙稳态破坏和自噬受损,这些都会导致细胞损伤。了解这些分子途径对于开发针对性的治疗干预措施以减轻热应激(HS)的影响至关重要。在我们探索众多治疗策略时,一种引人注目的分子引起了我们的关注:一氧化氮(NO)。这种无色气体主要由一氧化氮合酶(NOS)酶产生,在身体的各种功能中发挥着关键作用。从促进血管舒张和神经传递到调节免疫反应、血小板功能、细胞信号传导和生殖健康,NO因其多功能性而脱颖而出。将其作为热应激诱导的多器官损伤的一种有前景的治疗方法进行探索,凸显了其在有效治疗干预过程中的独特特征。这涉及探索药理学途径,考虑使用NO供体和抗氧化剂,以及非药理学策略,如采用富含硝酸盐的饮食和进行运动方案。本综述重点介绍了热应激的概念、该疾病的分子框架以及基于一些新干预措施的治疗选择。