Mitochondriopathy of peripheral arterial disease

Konstantinos I. Makris, Aikaterini A. Nella, Zhen Zhu, Stanley A. Swanson, George P. Casale, Tanuja L. Gutti, Andrew R. Judge, Iraklis I. Pipinos

Research output: Contribution to journalReview articlepeer-review

51 Scopus citations


The signs and symptoms of peripheral arterial occlusive disease (PAD), including claudication, rest pain, and tissue loss, are consequences of compromised bioenergetics and oxidative tissue injury within the affected lower extremities. Compromised bioenergetics is the result of a combination of low blood flow through diseased arteries and diminished adenosine triphosphate production by dysfunctional mitochondria. The tissue injury appears to be secondary to increased production of reactive oxygen species by dysfunctional mitochondria and by inflammation, in association with ischemia and ischemia/reperfusion. In this review, we present the current histomorphologic, physiologic, and biochemical evidence defining the nature of this mitochondriopathy and discuss its contribution to the pathogenesis and clinical manifestations of PAD.

Original languageEnglish (US)
Pages (from-to)336-343
Number of pages8
Issue number6
StatePublished - Nov 2007


  • Claudication
  • Energy metabolism
  • Ischemia
  • Mitochondria
  • Oxidative stress
  • Peripheral arterial disease
  • Skeletal muscle

ASJC Scopus subject areas

  • Surgery
  • Radiology Nuclear Medicine and imaging
  • Cardiology and Cardiovascular Medicine


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