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IMPAIRMENT OF PLATELET MITOCHONDRIAL RESPIRATION: AN OVERVIEW OF ANIMAL MODELS OF DISEASE AND DRUG-INDUCED TOXICITY

BOGDAN M. LOLESCU 1,2, ADINA V. FURDUI-LINȚA 1,2,3, MARIA D. DĂNILĂ 2,3, ALEXANDRU I. BLIDIȘEL 4, CRISTINA A. DEHELEAN 5, DANINA M. MUNTEAN 2,3, RODICA LIGHEZAN 6,7*, OCTAVIAN M. CREȚU 4

1Doctoral School Medicine, “Victor Babeș” University of Medicine and Pharmacy of Timișoara, Romania
2Centre for Translational Research and Systems Medicine, Faculty of Medicine, “Victor Babeș” University of Medicine and Pharmacy of Timișoara, Romania
3Department III – Chair of Pathophysiology, Faculty of Medicine, “Victor Babeș” University of Medicine and Pharmacy of Timișoara, Romania
4Department of Surgery I – Clinic of Surgical Semiotics & Thoracic Surgery, Centre for Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, “Victor Babeș” University of Medicine and Pharmacy of Timişoara, Romania
5Department I – Clinic of Toxicology, Drug Industry, Management & Legislation, Research Centre for Pharmaco-Toxicological Evaluation, Faculty of Pharmacy, “Victor Babeș” University of Medicine and Pharmacy of Timişoara, Romania
6Department XIII – Chair of Parasitology, Faculty of Medicine, “Victor Babeș” University of Medicine and Pharmacy of Timișoara, Romania
7Regional Blood Transfusion Centre, Timișoara, Romania

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Mitochondrial dysfunction is recognised as a central pathophysiological mechanism of most acute and chronic diseases. An emerging research field is represented by assessing the bioenergetic profile of peripheral blood cells (due to their accessibility) as a potential indicator of systemic mitochondrial dys/function. In particular, isolated platelets have been increasingly used for the ex vivo assessment of changes in mitochondrial respiration in animal disease models. Also, the past decades witnessed a growing interest in characterising the mechanisms underlying drug-induced mitochondrial toxicity to develop safer novel therapeutic agents, prevent their withdrawal from the market and test counteracting possibilities when mitochondrial toxicity has been demonstrated. In line with this, the modulation of platelet mitochondrial respiration by various pharmacological and toxic compounds has been increasingly tested in the field of mitochondrial toxicology.