Effects of statins on mitochondrial pathways — Research

Hamid Mollazadeh, PhD, Elmira Tavana, Giovanni Fanni, MD, Simona Bo, MD, Maciej Banach, MD PhD, Matteo Pirro, MD PhD, Stephan von Haehling, MD PhD, Tannaz Jamialahmadi, MD, Amirhossein Sahebkar, PhD · Narrative review

Many patients who stop statins do so over muscle aches. This review goes looking for a biological explanation, in the cell’s power plants — the mitochondria.

The authors assemble the mechanisms by which statins might disturb mitochondrial function: depleting coenzyme Q10 (whose synthesis the statin pathway can reduce), interfering with the respiratory chain, disrupting calcium handling, and raising oxidative stress. They connect these to the cluster of statin-associated complaints — muscle symptoms, a small diabetes risk, and cognitive concerns.

The practical takeaway is nuance, not alarm: understanding a plausible mechanism for statin side effects can help identify susceptible patients and rationalize mitigation strategies such as CoQ10 supplementation, without abandoning a drug class of proven benefit.

We rate the evidence moderate: a deep, 160-reference review spanning experimental and clinical work, critically assessed, though some authors carry conflicts and it is narrative rather than systematic. Its clinical significance is moderate — mechanistic insight relevant to managing real-world tolerability for the millions on statins. Read it alongside the large randomized evidence (Collins et al.) showing most reported muscle symptoms are nocebo: this review describes a real biological pathway without overturning the conclusion that statins’ benefits dominate for appropriate patients.