Preprint Review Version 1 This version is not peer-reviewed

Heat Shock Protein 60 as an Immunomodulator in Heart Diseases

Version 1 : Received: 1 August 2024 / Approved: 2 August 2024 / Online: 3 August 2024 (16:01:23 CEST)

How to cite: Saqagandomabadi, V.; Carista, A.; Di Felice, V. Heat Shock Protein 60 as an Immunomodulator in Heart Diseases. Preprints 2024, 2024080150. https://doi.org/10.20944/preprints202408.0150.v1 Saqagandomabadi, V.; Carista, A.; Di Felice, V. Heat Shock Protein 60 as an Immunomodulator in Heart Diseases. Preprints 2024, 2024080150. https://doi.org/10.20944/preprints202408.0150.v1

Abstract

The Characteristics of the cardiac muscle cell are described as a rod-shaped structure, single nu-cleus, and intercalated discs which make the heart’s action practical for enhancing contraction ef-ficiency. Mitochondria within these cells are vital for ATP synthesis, redox balance, calcium ho-meostasis, and lipid synthesis. The crucial role of Hsp60 is in protein folding and immune re-sponses; Hsp60 is a mitochondrial chaperonin, and its expression rises when the heart is under a stress condition like myocardial infarction and heart failure. This review has tried to deeply un-derstand the structural resemblance between cardiac and skeletal muscle cells, the amplitude number of mitochondria, its roles in cardiomyocytes, and the polyhedral functions of Hsp60. In this review, by investigating various articles, we brighten up Hsp60's distribution within cells, its association with apoptosis, and its action as a Damage Associated Molecular Pattern (DAMP), interacting with Toll-like receptors to modulate immune responses. Cardiac remodeling and failure are linked to cardiac-specific micro-RNAs whose expression may be affected by dysregu-lation of Hsp60. In conclusion, targeting mitochondrial function and Hsp60 expression may be of therapeutic potential for heart diseases.

Keywords

Heart; diseases; heat shock proteins; Hsp60; cardiac cells

Subject

Biology and Life Sciences, Anatomy and Physiology

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