Department of Physiology, Yerevan State Medical University named after Mkhitar Heratsi, Yerevan, Armenia.
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
J Investig Med. 2021 Aug;69(6):1148-1152. doi: 10.1136/jim-2020-001754. Epub 2021 May 5.
Growing evidence suggests an important role of the inflammatory component in heart failure (HF). Recent developments in this field indicate an ambiguous role that innate immunity plays in immune-driven HF. Damaged or stressed cells, cardiomyocytes, in particular, emit damage-associated molecular patterns (DAMPs) including HMGB1, S100 A8/A9, HSP70, and other molecules, unfolding paracrine mechanisms that induce an innate immune response. Designed as an adaptive, regenerative reaction, innate immunity may nevertheless become overactivated and thus contribute to the development of HF by altering the pacemaker rhythm, contraction, and electromechanical coupling, presumably by impairing the calcium homeostasis. The current review will explore a hypothesis of the involvement of the calcium-regulating hormones such as parathyroid hormone and parathyroid hormone-related protein in counteracting the detrimental impact of the excess of DAMPs and therefore improving the functional cardiac characteristics especially in the acute phase of the disease.
越来越多的证据表明，炎症成分在心力衰竭（HF）中起着重要作用。该领域的最新进展表明，固有免疫在免疫驱动的 HF 中起着复杂的作用。受损或应激细胞，特别是心肌细胞，会释放损伤相关分子模式（DAMPs），包括 HMGB1、S100A8/A9、HSP70 和其他分子，从而引发旁分泌机制，诱导固有免疫反应。固有免疫被设计为一种适应性、再生性反应，但它可能会过度激活，从而通过改变起搏节律、收缩和机电耦联来促进 HF 的发展，这可能是通过损害钙稳态来实现的。本综述将探讨钙调节激素（如甲状旁腺激素和甲状旁腺激素相关蛋白）参与对抗 DAMPs 过量的有害影响的假说，从而改善心脏功能特征，特别是在疾病的急性期。
