Far-Infrared Therapy　― Mechanisms of Action ―

Abstract

Far-infrared therapy, with wavelengths ranging from 3 to 25 μm, has emerged as a noninvasive photothermal and photobiomodulatory intervention with promising therapeutic applications in cardiovascular medicine, wound healing, and chronic inflammatory diseases. Far-infrared penetrates superficial and subcutaneous tissues, inducing mild, sustained hyperthermia and wavelength-specific molecular signaling. These effects activate mechanosensitive and thermosensitive pathways, including the transient receptor potential channels, phosphoinositide 3-kinase–Akt pathway, and adenosine monophosphate-activated protein kinase pathway. This activation leads to the phosphorylation of endothelial nitric oxide synthase, enhancing nitric oxide bioavailability and vascular homeostasis. In parallel, far-infrared attenuates oxidative stress by suppressing the activity of nicotinamide adenine dinucleotide phosphate oxidase, improving mitochondrial coupling, and activating the nuclear factor erythroid 2-related factor 2–antioxidant response element pathway, thereby increasing the expression of endogenous antioxidant enzymes. The resultant redox shift inhibits nuclear factor kappa B activation, reducing proinflammatory cytokine production, adhesion molecule expression, and leukocyte–endothelium interactions. Additionally, far-infrared promotes macrophage polarization toward an anti-inflammatory M2 phenotype and enhances angiogenic signaling, partly through vascular endothelial growth factor upregulation in a low-inflammatory milieu. Preclinical and clinical studies have shown that these combined antioxidant, anti-inflammatory, vasodilatory, and angiogenic effects contribute to improved microvascular perfusion, endothelial function, and tissue repair.