Data

Statin Associated Myopathy- Wistar Rat-Skeletal Muscles-Cardiac Muscles-Smooth Vascular Muscles

Central Queensland University
Kimberly Ryan (Aggregated by)
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ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Adc&rfr_id=info%3Asid%2FANDS&rft_id=info:doi10.25946/29511992.v1&rft.title=Statin Associated Myopathy- Wistar Rat-Skeletal Muscles-Cardiac Muscles-Smooth Vascular Muscles&rft.identifier=https://doi.org/10.25946/29511992.v1&rft.publisher=Central Queensland University&rft.description=Lifestyle choices such as inactivity and diets high in saturated fats has led to an increase in mortality associated with cardiovascular disease (CVD) in Australia. The main strategy to reduce CVD risk has been targeting elevations in cholesterol with a range of medications. Of these medications, statins or 3-hydroxy-3-methylglteryl coenzyme A reductase inhibitors are the most effective and most prescribed (S. Antonopoulos et al. 2012). Statins reduce low density lipoprotein concentrations (bad cholesterol) in circulation and formation within hepatic cells. Although statins are proficient at reducing CVD risk, side effects can develop and the most common is myopathy. Myopathy can range from muscle aches and pain to significant breakdown of skeletal muscle and is reported to affect 100 of every 1 000 000 statin patients (Gotto Jr 2006). Presently the mechanisms behind statin induced myopathy (SIM) are unknown and projects are underway to determine this, however what isn't know is how age and obesity impact upon its development. As such this study aims to investigate how aging and obesity impact upon the development of SIM. In addition to obtaining biometric data throughout the treatment period, terminal assessments of electrical and mechanical function of the heart will be undertaken, along with organ bath experiments examining the reactivity of small and large blood vessels and skeletal muscle function. Blood and tissue samples will also be collected for biochemical and molecular analysis in order to identify possible mechanisms by which SIM develops.&rft.creator=Kimberly Ryan&rft.date=2025&rft_rights=CC-BY-4.0&rft_subject=myopathy&rft_subject=statin&rft_subject=Pharmaceutical sciences&rft.type=dataset&rft.language=English Access the data

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Lifestyle choices such as inactivity and diets high in saturated fats has led to an increase in mortality associated with cardiovascular disease (CVD) in Australia. The main strategy to reduce CVD risk has been targeting elevations in cholesterol with a range of medications. Of these medications, statins or 3-hydroxy-3-methylglteryl coenzyme A reductase inhibitors are the most effective and most prescribed (S. Antonopoulos et al. 2012).

Statins reduce low density lipoprotein concentrations (bad cholesterol) in circulation and formation within hepatic cells. Although statins are proficient at reducing CVD risk, side effects can develop and the most common is myopathy. Myopathy can range from muscle aches and pain to significant breakdown of skeletal muscle and is reported to affect 100 of every 1 000 000 statin patients (Gotto Jr 2006). Presently the mechanisms behind statin induced myopathy (SIM) are unknown and projects are underway to determine this, however what isn't know is how age and obesity impact upon its development. As such this study aims to investigate how aging and obesity impact upon the development of SIM.

In addition to obtaining biometric data throughout the treatment period, terminal assessments of electrical and mechanical function of the heart will be undertaken, along with organ bath experiments examining the reactivity of small and large blood vessels and skeletal muscle function. Blood and tissue samples will also be collected for biochemical and molecular analysis in order to identify possible mechanisms by which SIM develops.


Issued: 2025-07-18

Created: 2025-07-18

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