What’s new in burns and metabolism

Sheridan, Robert L.; Tompkins, Ronald G.

doi:10.1016/j.jamcollsurg.2003.11.007

Cited by 50 publications

(37 citation statements)

References 321 publications

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“…When burn injury exceeds 30% of the total body surface area (TBSA), local inflammation generalizes into a severe systemic response metabolically characterized as muscle catabolism, leading to muscle wasting or 'cachexia' (1). While early burn wound excision has been shown to favorably influence the metabolic response and reduce catabolism (2), administration of appropriate factors that can change post-burn physiology would also be a powerful tool for ameliorating 'cachexia'.…”

Section: Introductionmentioning

confidence: 99%

Reduced rate of adenosine triphosphate synthesis by in vivo 31P nuclear magnetic resonance spectroscopy and downregulation of PGC-1β in distal skeletal muscle following burn

Tzika

Mintzopoulos²,

Padfield³

et al. 2008

Int J Mol Med

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Abstract. Using a mouse model of burn trauma, we tested the hypothesis that severe burn trauma corresponding to 30% of total body surface area (TBSA) causes reduction in adenosine triphosphate (ATP) synthesis in distal skeletal muscle. We employed in vivo 31 P nuclear magnetic resonance (NMR) in intact mice to assess the rate of ATP synthesis, and characterized the concomitant gene expression patterns in skeletal muscle in burned (30% TBSA) versus control mice. Our NMR results showed a significantly reduced rate of ATP synthesis and were complemented by genomic results showing downregulation of the ATP synthase mitochondrial F 1 F 0 complex and PGC-1ß gene expression. Our findings suggest that inflammation and muscle atrophy in burns are due to a reduced ATP synthesis rate that may be regulated upstream by PGC-1ß. These findings implicate mitochondrial dysfunction in distal skeletal muscle following burn injury. That PGC-1ß is a highly inducible factor in most tissues and responds to common calcium and cyclic adenosine monophosphate (cAMP) signaling pathways strongly suggests that it may be possible to develop drugs that can induce PGC-1ß.

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Section: Introductionmentioning

confidence: 99%

Reduced rate of adenosine triphosphate synthesis by in vivo 31P nuclear magnetic resonance spectroscopy and downregulation of PGC-1β in distal skeletal muscle following burn

Tzika

Mintzopoulos²,

Padfield³

et al. 2008

Int J Mol Med

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“…25 Intralesional injection and/or wound irrigation with interferon alfa-2b, interferon-γ, mitomycin C, bleomycin, or 5-fluorouracil seems to have a positive effect on the reduction of pathologic scars. [11][12][13][14][15][16] In this study, electroporation in combination with bleomycin has been applied for the first time to keloids and hypertrophic scars not responding to convention treatments. All lesions responded to the treatment and, 9 months after the first electrochemotherapy session, 94 percent of the lesions showed a volume reduction greater than 50 percent.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, even with state-of-the-art care (combining surgery, mechanical, and pharmacologic therapies), the results are still frustrating and "hypertrophic scarring remains a terrible clinical problem." 15 This is even more evident with lesions of large dimensions, when treatments are really hard for the patient and the outcome is often unsatisfactory.…”

mentioning

confidence: 99%

Treatment of Keloids and Hypertrophic Scars with Bleomycin and Electroporation

Manca

Pandolfi

Gregorelli

et al. 2013

Plastic and Reconstructive Surgery

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“…4 Proliferative scarring and chronic wounds in humans have adverse physical, aesthetic, functional, psychological, and social consequences. 6,7 The major aim of all wound healing technologies and treatments is to completely restore the function and structure of the wounded site to its initial condition.…”

Section: The Problem Of the Abnormal Wound Healing And Scarringmentioning

confidence: 99%

Scarless Tissue Regeneration

Golberg¹

2017

Frontiers in Nanobiomedical Research

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Wounds and wound healing are parts of every organism's life. What is a wound, how does it heal and what can we do to speed the healing, but decrease scarring? All these fundamental questions occupy the minds of people through all known history. Wound healing is an extremely complex phenomenon, which involves both the organism and its environment. Moreover, chemical, biological, mechanical and electrical forces drive this phenomenon. This chapter attempts to combine various aspects of wound healing phenomena with an emphasis on scarless regeneration. The system approach to wound healing is needed to develop new therapies. This chapter starts with the general overview on what is a wound from the system perspective. Then it describes the highlevel events that take place during normal and abnormal wound healing. Next, it gives a historic perceptive on the history of wound healing in humans. Then it describes the fundamentals of scar biology, going to the details of known biochemical and cellular events involved in the process of scar formation. It then deals with the mechanical and electrical events that affect wound healing process. Next, complex events such as inflammation and wound-bacteria interaction are discussed, followed by descriptions of the in vitro and in vivo models of scarless wound healing. This chapter concludes with open questions and future perspectives of scarless wound healing.

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What’s new in burns and metabolism

Cited by 50 publications

References 321 publications

Reduced rate of adenosine triphosphate synthesis by in vivo 31P nuclear magnetic resonance spectroscopy and downregulation of PGC-1β in distal skeletal muscle following burn

Reduced rate of adenosine triphosphate synthesis by in vivo 31P nuclear magnetic resonance spectroscopy and downregulation of PGC-1β in distal skeletal muscle following burn

Treatment of Keloids and Hypertrophic Scars with Bleomycin and Electroporation

Scarless Tissue Regeneration

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