Photobiomodulation (PBM), a noninvasive phototherapy that utilizes wavelengths between red and near-infrared light, has emerged as a promising approach for controlling inflammation by modulating macrophage polarization. This review investigates the therapeutic potential of PBM in treating ENT-specific inflammatory conditions, such as chronic rhinosinusitis and otitis media, focusing on its effects on macrophage phenotypes and evidence from preclinical studies. By promoting mitochondrial activity, increasing adenosine triphosphate production, and modulating reactive oxygen species, PBM has been shown to shift macrophages from a pro-inflammatory to an anti-inflammatory phenotype. Studies have demonstrated that PBM enhances tissue repair, reduces inflammatory markers, and promotes wound healing. Moreover, PBM facilitates the polarization of M2 macrophages, a crucial factor in resolving mucosal inflammation in the nasal, pharyngeal, and middle ear cavities, as well as restoring tissue homeostasis. The anti-inflammatory effects of PBM are attributed to its ability to influence several molecular mechanisms involved in inflammation regulation, particularly in ENT organ tissues, where recurrent inflammation can lead to chronic conditions such as otitis media or sinusitis. Furthermore, this review compares PBM to competing methods for reprogramming macrophages and treating inflammation, highlighting its advantages of minimal toxicity, simplicity, and precision in controlling ENT immune responses.

Photobiomodulation (PBM), a noninvasive phototherapy that utilizes wavelengths between red and near-infrared light, has emerged as a promising approach for controlling inflammation by modulating macrophage polarization. This review investigates the therapeutic potential of PBM in treating ENT-specific inflammatory conditions, such as chronic rhinosinusitis and otitis media, focusing on its effects on macrophage phenotypes and evidence from preclinical studies. By promoting mitochondrial activity, increasing adenosine triphosphate production, and modulating reactive oxygen species, PBM has been shown to shift macrophages from a pro-inflammatory to an anti-inflammatory phenotype. Studies have demonstrated that PBM enhances tissue repair, reduces inflammatory markers, and promotes wound healing. Moreover, PBM facilitates the polarization of M2 macrophages, a crucial factor in resolving mucosal inflammation in the nasal, pharyngeal, and middle ear cavities, as well as restoring tissue homeostasis. The anti-inflammatory effects of PBM are attributed to its ability to influence several molecular mechanisms involved in inflammation regulation, particularly in ENT organ tissues, where recurrent inflammation can lead to chronic conditions such as otitis media or sinusitis. Furthermore, this review compares PBM to competing methods for reprogramming macrophages and treating inflammation, highlighting its advantages of minimal toxicity, simplicity, and precision in controlling ENT immune responses.

Photobiomodulation (PBM), a noninvasive phototherapy that utilizes wavelengths between red and near-infrared light, has emerged as a promising approach for controlling inflammation by modulating macrophage polarization. This review investigates the therapeutic potential of PBM in treating ENT-specific inflammatory conditions, such as chronic rhinosinusitis and otitis media, focusing on its effects on macrophage phenotypes and evidence from preclinical studies. By promoting mitochondrial activity, increasing adenosine triphosphate production, and modulating reactive oxygen species, PBM has been shown to shift macrophages from a pro-inflammatory to an anti-inflammatory phenotype. Studies have demonstrated that PBM enhances tissue repair, reduces inflammatory markers, and promotes wound healing. Moreover, PBM facilitates the polarization of M2 macrophages, a crucial factor in resolving mucosal inflammation in the nasal, pharyngeal, and middle ear cavities, as well as restoring tissue homeostasis. The anti-inflammatory effects of PBM are attributed to its ability to influence several molecular mechanisms involved in inflammation regulation, particularly in ENT organ tissues, where recurrent inflammation can lead to chronic conditions such as otitis media or sinusitis. Furthermore, this review compares PBM to competing methods for reprogramming macrophages and treating inflammation, highlighting its advantages of minimal toxicity, simplicity, and precision in controlling ENT immune responses.

Photobiomodulation (PBM) is emerging as a non-invasive modality that modulates cellular metabolism and signaling through the application of red and near-infrared light. While extensively studied for its regenerative applications, such as wound healing and skin rejuvenation, PBM’s impact on cancer cells and its potential role as an adjunct in cancer treatment have drawn increasing attention. This review critically examines the molecular mechanisms by which PBM influences cancer cell behavior, including its effects on mitochondrial function, reactive oxygen species modulation, and gene expression, and discusses the dualistic nature of PBM in oncology. Preclinical studies, particularly those utilizing glioblastoma cell lines, reveal both anti-apoptotic and anti-proliferative effects while emerging data support the promising yet complex use of PBM in combination with conventional treatments such as chemotherapy and radiotherapy. Finally, the challenges in optimizing the light parameters for safe application in oncologic settings are addressed, along with future research directions to harness PBM’s full therapeutic potential while avoiding inadvertent tumor stimulation.

Photobiomodulation (PBM), the application of redear-infrared light (600-1,000 nm) on cells, modulates cellular bioenergetics and immune signaling without thermal injury. This review presents mechanistic, preclinical, and clinical studies to clarify how wavelength, irradiance, and dose shape immune outcomes and outlines the therapeutic implications. Mechanistically, PBM accelerates mitochondrial electron transport and adenosine triphosphate production, tunes reactive oxygen species biphasically, and engages the nuclear factor kappalight-chain-enhancer of activated B cells, mitogen-activated protein kinase, and nuclear factor erythroid 2-related factor 2 pathways to reprogram inflammatory gene expression. Across lineages, PBM promotes macrophage polarization toward reparative phenotypes, limits neutrophil recruitment and degranulation, supports dendritic cell maturation and antigen presentation, and recalibrates T cell responses by expanding regulatory T cells and shifting T helper type 1 (Th1)/Th2/Th17 balance toward homeostasis. These effects translate into benefits in wound repair, arthritis, neuroinflammation, and select autoimmune conditions, and suggest combinability with vaccines, biologics, and cancer immunotherapies. Despite a favorable safety profile, heterogeneity in irradiance, fluence, duty cycle, and schedules hinders comparison and adoption. This review highlights the need for better reporting standards and condition-specific dosing windows anchored to target cell type, depth, and redox state. This can enable biomarker-guided trials that integrate immune phenotyping with clinical and safety endpoints.Photobiomodulation (PBM), the application of redear-infrared light (600-1,000 nm) on cells, modulates cellular bioenergetics and immune signaling without thermal injury. This review presents mechanistic, preclinical, and clinical studies to clarify how wavelength, irradiance, and dose shape immune outcomes and outlines the therapeutic implications. Mechanistically, PBM accelerates mitochondrial electron transport and adenosine triphosphate production, tunes reactive oxygen species biphasically, and engages the nuclear factor kappalight-chain-enhancer of activated B cells, mitogen-activated protein kinase, and nuclear factor erythroid 2-related factor 2 pathways to reprogram inflammatory gene expression. Across lineages, PBM promotes macrophage polarization toward reparative phenotypes, limits neutrophil recruitment and degranulation, supports dendritic cell maturation and antigen presentation, and recalibrates T cell responses by expanding regulatory T cells and shifting T helper type 1 (Th1)/Th2/Th17 balance toward homeostasis. These effects translate into benefits in wound repair, arthritis, neuroinflammation, and select autoimmune conditions, and suggest combinability with vaccines, biologics, and cancer immunotherapies. Despite a favorable safety profile, heterogeneity in irradiance, fluence, duty cycle, and schedules hinders comparison and adoption. This review highlights the need for better reporting standards and condition-specific dosing windows anchored to target cell type, depth, and redox state. This can enable biomarker-guided trials that integrate immune phenotyping with clinical and safety endpoints.

Photobiomodulation (PBM) is a novel approach in regenerative medicine that utilizes red and near-infrared light to enhance wound healing and skin regeneration by regulating crucial cellular processes. This noninvasive therapy stimulates mitochondrial activity, balances reactive oxygen species, and regulates gene expression to increase fibroblast proliferation, angiogenesis, keratinocyte migration, and collagen remodeling. PBM’s applications range from faster recovery of patients with burns and diabetic ulcers to improved cosmetic outcomes through skin rejuvenation and reduced scarring. Unlike traditional treatments, PBM addresses the multifaceted challenges of wound healing, such as prolonged inflammation and suboptimal tissue repair, by simultaneously targeting multiple pathways. Despite its transformative potential, challenges remain, such as standardizing treatment protocols and refining mechanistic understanding. With the advancement of light delivery technologies and multimodal applications, PBM is poised to become a cornerstone therapy for enhancing tissue repair across diverse clinical settings. This review provides current insights into the mechanisms, therapeutic applications, and future directions of PBM, highlighting its integral role in advancing wound care and skin regeneration.

Photobiomodulation (PBM) therapy, using red to near-infrared light (600-1,000 nm), is becoming a promising non-invasive treatment for neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. This review examines the mechanistic insights and the preclinical and clinical evidence supporting the efficacy of PBM in enhancing mitochondrial function, reducing oxidative stress, and modulating neuroinflammation. The impact of PBM therapy on cellular energy production, gene expression, and inflammatory responses provides a comprehensive therapeutic approach targeting multiple pathological pathways in neurodegenerative conditions. Preclinical studies demonstrated the potential of PBM therapy in improving neuronal health and cognitive function, while early clinical trials revealed significant benefits in motor performance and cognitive outcomes with minimal adverse effects. By highlighting the necessity for personalized PBM therapy and its integration with other therapeutic modalities, the literature aims to optimize the treatment efficacy and expand the clinical applications of PBM technology. Further large-scale randomized controlled trials are essential to validate these findings and establish standardized treatment protocols, as current promising results position PBM as a viable and innovative therapeutic option for managing and potentially altering the course of neurodegenerative diseases.

Mitochondrial dysfunction is a critical factor in the pathogenesis of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis. Disruptions in mitochondrial fusion and fission lead to the accumulation of damaged mitochondria and elevated oxidative stress, contributing to neuronal cell death. Photobiomodulation (PBM) therapy, utilizing low-level laser light or light-emitting diodes, has shown promise in restoring mitochondrial dynamics by stimulating cytochrome c oxidase in the mitochondrial respiratory chain. This enhances adenosine triphosphate production, promotes mitochondrial fusion, and reduces fission. Additionally, PBM attenuates neuroinflammation by reducing pro-inflammatory cytokine and reactive oxygen species production, creating a favorable environment for neuronal survival. This review explores the mechanisms through which PBM influences mitochondrial dynamics and its therapeutic potential in neurodegenerative diseases. By restoring mitochondrial balance and reducing neuroinflammation, PBM offers a unique approach to mitigating mitochondrial dysfunction and enhancing neuronal function.

The first edition of the guidelines for the use of ultrasound contrast agents was published in 2004, dealing with liver applications. The second edition of the guidelines in 2008 reflected changes in the available contrast agents and updated the guidelines for the liver, as well as implementing some nonliver applications. The third edition of the contrast-enhanced ultrasound (CEUS) guidelines was the joint World Federation for Ultrasound in Medicine and Biology-European Federation of Societies for Ultrasound in Medicine and Biology (WFUMB-EFSUMB) venture in conjunction with other regional US societies such as Asian Federation of Societies for Ultrasound in Medicine and Biology, resulting in a simultaneous duplicate on liver CEUS in the official journals of both WFUMB and EFSUMB in 2013. However, no guidelines were described mainly for Sonazoid due to limited clinical experience only in Japan and Korea. The new proposed consensus statements and recommendations provide general advice on the use of Sonazoid and are intended to create standard protocols for the use and administration of Sonazoid in hepatic and pancreatobiliary applications in Asian patients and to improve patient management.

The nuclear hormone receptor PPARgamma is activated by several agonists, including members of the thiazolidinedione group of insulin sensitizers. Pleiotropic beneficial effects of these agonists, independent of their blood glucose-lowering effects, have recently been demonstrated in the vasculature. PPARgamma agonists have been shown to lower blood pressure in animals and humans, perhaps by suppressing the renin-angiotensin (Ang)-aldosterone system (RAAS), including the inhibition of Ang II type 1 receptor expression, Ang-II-mediated signaling pathways, and Ang-II-induced adrenal aldosterone synthesis/secretion. PPARgamma agonists also inhibit the progression of atherosclerosis in animals and humans, possibly through a pathway involving the suppression of RAAS and the thromboxane A2 system, as well as the protection of endothelial function. Moreover, PPARgamma-agonist-mediated renal protection, especially the reduction of albuminuria, has been observed in diabetic nephropathy, including animal models of the disease, and in non-diabetic renal dysfunction. The renal protective activities may reflect, at least in part, the ability of PPARgamma agonists to lower blood pressure, protect endothelial function, and cause vasodilation of the glomerular efferent arterioles. Additionally, anti-neoplastic effects of PPARgamma agonists have recently been described. Based on the multiple therapeutic actions of PPARgamma agonists, they will no doubt lead to novel approaches in the treatment of lifestyle-related and other diseases.
Animals ; Atherosclerosis/prevention & control ; Humans ; Hypertension/drug therapy ; Hypoglycemic Agents/*pharmacology ; Kidney Diseases/etiology ; PPAR gamma/*agonists ; PPAR-beta/agonists