Re:Heat Shock Protein과 당뇨, 상처치유에 관한 논문

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열충격 단백질은 어디까지 영향을 미치는 걸까? 도대체

HEAT SHOCK PROTEINS IN DIABETES AND WOUND HEALING.pdf

HEAT SHOCK PROTEINS IN DIABETES AND WOUND HEALING

Mustafa Atalay1, Niku Oksala1,2, Jani Lappalainen1,3, David E. Laaksonen1,4, Chandan K.

Sen5, and Sashwati Roy5

1 Institute of Biomedicine, Physiology, University of Kuopio, Finland 2 Department of Surgery,

Tampere University Hospital, Finland 3 Wihuri Research Institute, Helsinki, Finland 4 Institute of

Clinical Medicine, Internal Medicine, University of Kuopio, Kuopio, Finland 5 Comprehensive Wound

Center, Department of Surgery, Dorothy M. Davis Heart & Lung Research Institute, The Ohio State

University Medical Center, Columbus, OH, USA

Abstract

The heat shock proteins (HSPs), originally identified as heat-inducible gene products, are a highly conserved family of proteins that respond to a wide variety of stress. Although HSPs are among the most abundant intracellular proteins, they are expressed at low levels under normal physiological conditions, and show marked induction in response to various stressors. 

HSPs function primarily as molecular chaperones, facilitating the folding of other cellular proteins, preventing protein aggregation, or targeting improperly folded proteins to specific pathways for degradation. By modulating inflammation, wound debris clearance, cell proliferation, migration and collagen synthesis, HSPs are essential for normal wound healing of the skin. 

In this review, our goal is to discuss the role and clinical implications of HSP with respect to skin wound healing and diabetes. The numerous defects in the function of HSPs associated with diabetes could contribute to the commonly observed complications and delayed wound healing in diabetics. Several physical, pharmacological and genetic approaches may be considered to address HSP-directed therapies both in the laboratory and in the clinics.

Schematic presentation of the regulation, mechanisms, inducers and inhibitors of heat shock protein (HSP) synthesis and the effect of HSPs on key factors in wound healing. Physical inducers include heat shock, ischemia-reperfusion, physical exercise, heavy metals, toxins, radiation, UV-light, laser, decreased ATP levels, pH and osmolarity changes. Pharmacological inducers include bimoclomol, geranylgeranylacetone (GGA), α-lipoic acid, ansamycins, butyrate, prostaglandins, celastrol, terrecyclin-A, BRX-220, PLA2 and nitric oxide (NO). Solid lines represent stimulation and dashed lines inhibition. Dot lines represent both stimulation and inhibition. HSF, heat shock factor; HSE, heat shock element; NF-κB, nuclear factor-κB; eEFs, eukaryotic elongation factors; eIFs, eukaryotic translation initiation factors.

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