Last updated: July 2026 · Written by the Dermfix phototherapy team
Short answer: Red and near-infrared light is absorbed by an enzyme called cytochrome c oxidase inside your mitochondria — the cell's energy factories. This absorption kicks off a chain reaction: more ATP (cellular energy) gets made, nitric oxide gets released, calcium levels shift, and a cascade of signals reaches the cell's nucleus, switching on genes tied to healing, reduced inflammation, and cell survival. It's a real, mapped biological pathway — not a vague “energy” claim.
The review
Lucas Freitas de Freitas (University of São Paulo) and Michael R. Hamblin (Harvard Medical School's Wellman Center for Photomedicine) co-authored this comprehensive mechanistic review, published in IEEE Journal of Selected Topics in Quantum Electronics in 2016. Hamblin is one of the most cited researchers in the photobiomodulation field, and this paper pulls together decades of molecular and cellular research into a single account of how low-level light therapy (LLLT), also called photobiomodulation (PBM), actually works.
The starting point: an enzyme called cytochrome c oxidase
The central player in this whole process is cytochrome c oxidase — an enzyme sitting in the mitochondrial membrane that's the last stop in the chain of reactions your cells use to produce energy. It happens to absorb light strongly in the red and near-infrared range, which is why those wavelengths are the ones used in phototherapy.
The leading explanation for what happens next: light knocks loose a molecule of nitric oxide that had been sitting on the enzyme and inhibiting it. With that blockage removed, electron transport speeds up, the mitochondria's membrane potential rises, and ATP production increases. In simple terms — the cell's power plant, which was partially jammed, gets unstuck and starts running more efficiently.
A second, less-established pathway involves light-sensitive channels in the cell membrane called TRP channels, which can open in response to certain wavelengths and let calcium flow into the cell — triggering its own set of downstream effects.
From one enzyme to whole-body effects
What makes this interesting isn't just the initial reaction — it's what happens afterward. The paper describes a cascade: increased ATP and shifts in nitric oxide, reactive oxygen species, and calcium act as internal messengers that reach the cell's nucleus and activate transcription factors — proteins that switch genes on or off. These downstream effects include:
- Reduced inflammation — via changes in cytokine signaling and heat-shock proteins
- Increased cell migration and proliferation — relevant to wound healing and tissue repair
- Anti-apoptotic signaling — helping stressed cells survive rather than die off
- Increased antioxidant enzyme activity — helping cells manage oxidative stress
- Growth factor release — including factors tied to collagen production and blood vessel formation
The paper also highlights that stem cells and progenitor cells appear to be particularly responsive to this kind of light stimulation, showing increased proliferation, migration, and differentiation — a finding with implications well beyond skin, touching on bone, muscle, and nerve regeneration research.
Dose still rules everything
As with the other research in this space, dose is central. The paper describes the same biphasic, “Arndt-Schulz” pattern seen throughout the LLLT literature: too little light does nothing, a moderate dose stimulates cells, and too much light suppresses or even damages them. The authors cite research showing effects that stimulate proliferation at low doses (up to roughly 2 J/cm²) but flip to suppressive at higher doses (16 J/cm² and above) — underscoring why “more light” isn't a reliable strategy and why device parameters matter as much as simply having a red light source.
Interestingly, the review also notes that irradiance (the intensity of light delivered per second) can matter independently of total energy density — several cited studies found that delivering the same total dose at different intensities produced different biological outcomes, which is part of why dosing protocols in this field remain an active area of research.
Coherence, once again, isn't the deciding factor
Consistent with other research in this space, the authors note that the belief that coherent laser light was necessary for these effects is no longer widely held — non-coherent LED sources have been shown to be similarly effective at triggering the same cytochrome c oxidase-driven pathway.
Frequently asked questions
What's the single most important target of red/NIR light in cells?
Cytochrome c oxidase, an enzyme in the mitochondria that's the leading candidate for how light triggers these biological effects.
Does more light dose mean a stronger effect?
No — the research consistently shows a biphasic response: effects build with dose up to a point, then plateau and reverse at excessive doses.
Why does this matter for something like wound healing or muscle recovery?
Because the same downstream signaling cascade — increased ATP, reduced inflammation, growth factor release, and enhanced cell migration — is the biological basis connecting light exposure to visible outcomes like faster healing.
Is this mechanism fully settled science?
The core cytochrome c oxidase / nitric oxide pathway is the leading, best-supported hypothesis, but the authors are clear that several complementary mechanisms (light-sensitive ion channels, direct effects on other molecules) are still being actively researched, and the complete picture isn't finalized.
Sourced from: de Freitas, L.F. & Hamblin, M.R. “Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy.” IEEE Journal of Selected Topics in Quantum Electronics, 22(3), 2016. DOI: 10.1109/JSTQE.2016.2561201.
Disclaimer: this article summarises published research for general information. It is not medical advice and does not describe the intended purpose of any Dermfix product.