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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Burns. 2016 Jan 17;42(5):1025–1035. doi: 10.1016/j.burns.2015.11.007

Table 1.

Studies examining burn wound progression from 2010 to 2014

Mechanism Author(s) Year Animal Model Burn Model Conclusions
Autophagy Tan et al. 2013 Murine Comb model Autophagy contributes to cell death in zone of stasis; autophagy and apoptosis peak at different time intervals
Xiao et al. 2013 Murine Heated brass rod Induction of autophagy (with rapamycin) decreases burn wound progression and improves wound healing
Xiao et al. 2014 Murine Heated brass rod Autophagy is decreased and apoptosis is increased early in the course of burn progression in deep second-degree burns
Inflammation Begieneman et al. 2012 Murine Heated copper stamp Long term treatment with a C1 inhibitor post-burn improves wound healing and decreases local inflammation, particularly macrophage infiltration
Bohr et al.* 2013 Murine Comb model, scald burn Resolvin D2 prevents thrombosis of the DDVN, TNF-α secretion and secondary burn progression; Resolvin D2 does not reduce PMN infiltration
Eski et al. 2011 Murine Comb model Cerium nitrate baths immediately after burn injury prevent progressive tissue necrosis in the zone of stasis
Friedrich et al. 2013 Murine Heated brass disk TNF-α conjugated to HA more effectively prevent burn progression and decrease inflammatory markers compared to TNF-α alone or mixed with HA
Rizzo et al. 2013 Murine Comb model Systemic hypothermia after thermal injury decreases levels of tissue remodeling genes, increase expression of skin protective genes and reduce burn conversion
Singer et al.** 2011 Murine Comb model Curcumin reduces burn wound progression when administered after burn injury
Sun et al. 2012 Murine Heated brass disk Topical antibodies to TNF-α, but not IL-6, reduce burn wound progression
Ischemia Bohr et al. 2013 Murine Scald burn Alternative EPO-mediated signaling lessens TNF-α secretion, decreases microvascular thrombosis and reduces burn wound conversion
Fourman et al. 2013 Porcine Comb burn model ICG angiography delineates viable versus noviable tissue in the zone of injury up to 1 hour post-burn
Hirth et al. 2013 Porcine Heated aluminum bar Endothelial cell necrosis at 1 hour post burn is predictive of apoptosis at 24 hours and tissue necrosis at 7 days; the zone of stasis is comprised of two vertically-divided subzones based on endothelial cell necrosis
Tobalem et al. 2012 Murine Comb model Early (45 minute), but not late (6 hour) EPO treatment post-burn decreases burn progression
Tobalem et al. 2013 Murine Comb model EPO decreases secondary burn progression in a dose-dependent manner, independent of iNOS expression, anti-inflammatory or angiogenic effects
Tobalem et al. 2013 Murine Comb model Immediate application of warm water to burn wounds improves early perfusion and decreases zone of stasis necrosis
Yuhua et al. 2012 Murine Heated brass rod Systemic treatment with Poloxamer 188 reduces burn wound progression in deep second-degree burns
ROS Deniz et al. 2013 Murine Comb model N-acetylcysteine prevents secondary tissue necrosis in the zone of stasis
Shalom et al. 2011 Murine Comb model Prophyalactic treatment with recombinant copper-zinc SOD does not improve zone of stasis survival
Other Macri et al. 2013 Porcine Comb model Immediate burn excision does not prevent burn progression in surrounding zone of stasis
Oksuz et al. 2013 Murine Comb model Subcutaneous MSC injections 30 minutes post-burn decrease apoptosis in the zone of stasis and necrosis in the zone of stasis
Singer et al. 2010 Porcine Comb model Bromelain-based enzymatic debridement of burn eschar reduces tissue necrosis in the zone of stasis compared to controls
Singer et al. 2013 Murine Comb model Systemic MSC treatment 1 hour after burn injury reduces necrosis in the zone of stasis by around 20%
Turkaslan et al. 2010 Murine Comb model HBOT increases cells in the proliferative phase at 24 hours post-burn, increases tissue perfusion at 5 days post-burn, and decreases secondary necrosis in the zone of stasis

PMN, Polymorphonuclear neutrophil; TNF-α, Tumor necrosis factor-alpha; HA, Hyaluronic acid; IL-6, Interleukin-6; ICG, Indocyanine green; EPO, Erythropoietin; iNOS, Inducible nitric oxide synthase; HBOT, Hyperbaric oxygen treatment; ROS, Reactive oxygen species; SOD, Superoxide dismutase; MSC, Mesenchymal stem cell.

Study also addressed *ischemia, **ROS, and inflammation