Next Article in Journal
Long-Term Effects of Pregnancy Complications on Maternal Health: A Review
Next Article in Special Issue
Use of FGF-21 as a Biomarker of Mitochondrial Disease in Clinical Practice
Previous Article in Journal
The Role of Th17 Cells in the Pathogenesis of Behcet’s Disease
Previous Article in Special Issue
Evidence of Oxidative Stress and Secondary Mitochondrial Dysfunction in Metabolic and Non-Metabolic Disorders
Open AccessFeature PaperReview

Statins, Muscle Disease and Mitochondria

Departments of Chemical Pathology/Metabolic Medicine, Guys and St Thomas’ Hospitals NHS Foundation Trust, London SE1 7EH, UK
Adult Inherited Metabolic Diseases, Centre for Inherited Metabolic Diseases, Evelina, Guys and St Thomas’ Hospitals NHS Foundation Trust, Lambeth Palace Road, London SE1 7EH, UK
Author to whom correspondence should be addressed.
Academic Editors: Iain P. Hargreaves and Jane Grant-Kels
J. Clin. Med. 2017, 6(8), 75;
Received: 6 May 2017 / Revised: 28 June 2017 / Accepted: 12 July 2017 / Published: 25 July 2017
Cardiovascular disease (CVD) accounts for >17 million deaths globally every year, and this figure is predicted to rise to >23 million by 2030. Numerous studies have explored the relationship between cholesterol and CVD and there is now consensus that dyslipidaemia is a causal factor in the pathogenesis of atherosclerosis. Statins have become the cornerstone of the management of dyslipidaemia. Statins have proved to have a very good safety profile. The risk of adverse events is small compared to the benefits. Nevertheless, the potential risk of an adverse event occurring must be considered when prescribing and monitoring statin therapy to individual patients. Statin-associated muscle disease (SAMS) is by far the most studied and the most common reason for discontinuation of therapy. The reported incidence varies greatly, ranging between 5% and 29%. Milder disease is common and the more serious form, rhabdomyolysis is far rarer with an incidence of approximately 1 in 10,000. The pathophysiology of, and mechanisms leading to SAMS, are yet to be fully understood. Literature points towards statin-induced mitochondrial dysfunction as the most likely cause of SAMS. However, the exact processes leading to mitochondrial dysfunction are not yet fully understood. This paper details some of the different aetiological hypotheses put forward, focussing particularly on those related to mitochondrial dysfunction. View Full-Text
Keywords: cardiovascular; statin; myopathy; muscle; mitochondria cardiovascular; statin; myopathy; muscle; mitochondria
Show Figures

Figure 1

MDPI and ACS Style

Ramachandran, R.; Wierzbicki, A.S. Statins, Muscle Disease and Mitochondria. J. Clin. Med. 2017, 6, 75.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop