A Role for Photobiomodulation in the Prevention of Myocardial Ischemic Reperfusion Injury: A Systematic Review and Potential Molecular Mechanisms.
Myocardial ischemia reperfusion injury is a negative pathophysiological event that may result in cardiac cell apoptosis and is a result of coronary revascularization and cardiac intervention procedures. The resulting loss of cardiomyocyte cells and the formation of scar tissue, leads to impaired heart function, a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation is a novel cardiac intervention that has displayed therapeutic effects in reducing myocardial ischemia reperfusion related myocardial injury in animal models. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models has implicated multiple molecular interactions. A systematic review was conducted to identify the strength of the evidence for the therapeutic effect of photobiomodulation and to summarise the current evidence as to its mechanisms. Photobiomodulation in animal models showed consistently positive effects over a range of wavelengths and application parameters, with reductions in total infarct size (up to 76%), decreases in inflammation and scarring, and increases in tissue repair. Multiple molecular pathways were identified, including modulation of inflammatory cytokines, signalling molecules, transcription factors, enzymes and antioxidants. Current evidence regarding the use of photobiomodulation in acute and planned cardiac intervention is at an early stage but is sufficient to inform on clinical trials.
Australasian Research Institute, Wahroonga, Australia.|Sydney University, Sydney, Australia.
Ann
A
Liebert
Maitland Hospital, Maitland, Australia.
Andrew
A
Krause
Sydney University, Sydney, Australia.|Blacktown Hospital, Sydney, Australia.
Neil
N
Goonetilleke
Australasian Research Institute, Wahroonga, Australia.|Australian Catholic University, North Sydney, Australia.
Brian
B
Bicknell
University of New South Wales, Kensington, Australia.|Macquarie University, Marsfield, Australia.
Hosen
H
Kiat
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D015982:Bias; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003599:Cytoskeleton / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D028022:Low-Level Light Therapy; D008928:Mitochondria / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control* / Q000532:radiotherapy*; D010084:Oxidation-Reduction; D012306:Risk; D015398:Signal Transduction; D013997:Time Factors
D000975:Antioxidants; D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; D036341:Intercellular Signaling Peptides and Proteins