PT - JOURNAL ARTICLE AU - Satenik H Adamyan AU - Knarik R Harutyunyan AU - Hermine T Abrahamyan AU - Drastamat N Khudaverdyan AU - Souren Mkrtchian AU - Anna S Ter-Markosyan TI - Can the calcium-regulating hormones counteract the detrimental impact of pro-inflammatory damage-associated molecular patterns in the development of heart failure? AID - 10.1136/jim-2020-001754 DP - 2021 Aug 01 TA - Journal of Investigative Medicine PG - 1148--1152 VI - 69 IP - 6 4099 - http://hw-f5-jim.highwire.org/content/69/6/1148.short 4100 - http://hw-f5-jim.highwire.org/content/69/6/1148.full SO - J Investig Med2021 Aug 01; 69 AB - 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.