Key result
Statin therapy lowers ASCVD risk but may theoretically trigger intracellular morbidities via cellular cholesterol influx.
This perspective highlights the theoretical risk of intracellular cholesterol accumulation and associated morbidities resulting from statin-induced LDL receptor upregulation.
Statins retards intracellular biosynthesis of cholesterol by inhibiting HMG‐CoA reductase, increases low density lipoprotein (LDL) receptor (LDLR) expression and enhances LDL clearance rate through LDLRs. This reduces atherosclerotic tenor within the blood vessels showing the beneficial effect of statin drugs. On the other hand, incessant import into cell cytoplasm promotes chances to saturate cholesterol in organ or organelle(s). This organ or organelle is presumed to be inclined to unprecedented pathological abnormalities like upset of cell cycle regulation in cell nucleus, cholesterol storage disorder in lysosome and mitochondria, and diabetic onset in pancreas. While within the blood vessel the action of statin is therapy friendly by reducing cholesterol level; statin may also be accountable in casting intracellular morbidities by creating an environment of non‐stop cholesterol entry. The spectrum of these harmful side effects by different types of statins (lipophilic/hydrophilic) are still remained unexplored offering an open area for future therapeutic interests.
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Chandra et al. (2026) conducted a review in Cholesterol Homeostasis. Statin Therapy was evaluated. Statin therapy reduces atherosclerotic risk but may theoretically cause intracellular morbidities by promoting continuous cholesterol entry into cells.
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