Prevention of diabetes-induced microangiopathy by human tissue kallikrein gene transfer

Circulation. 2002 Aug 20;106(8):993-9. doi: 10.1161/01.cir.0000027104.33206.c8.

Abstract

Background: Microvascular insufficiency represents a major cause of end-organ failure among diabetics.

Methods and results: In streptozotocin-induced diabetic mice, we evaluated the potential of human tissue kallikrein (hTK) gene as a sole therapy against peripheral microangiopathy. Local delivery of hTK gene halted the progression of microvascular rarefaction in hindlimb skeletal muscle by inhibiting apoptosis, thus ensuring an improved hemodynamic recovery in case of supervening vascular occlusion. The curative action of hTK did not necessitate insulin supplementation. Application of gene therapy at a stage of established microangiopathy stimulated vascular regeneration.

Conclusions: Our studies indicate that hTK may represent a useful tool for the treatment of microvascular complications in diabetics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Combined Modality Therapy
  • Diabetes Mellitus, Experimental / complications*
  • Diabetic Angiopathies / etiology
  • Diabetic Angiopathies / pathology
  • Diabetic Angiopathies / prevention & control*
  • Genetic Therapy*
  • Hindlimb / blood supply
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Insulin / therapeutic use
  • Ischemia / etiology
  • Ischemia / pathology
  • Ischemia / prevention & control*
  • Kinetics
  • Male
  • Mice
  • Microcirculation / drug effects
  • Microcirculation / pathology
  • Muscle, Skeletal / blood supply
  • Muscle, Skeletal / chemistry
  • Muscle, Skeletal / pathology
  • Nucleotides, Cyclic / analysis
  • Tissue Kallikreins / genetics*

Substances

  • Hypoglycemic Agents
  • Insulin
  • Nucleotides, Cyclic
  • Tissue Kallikreins