Current Research · Aesthetic Medicine

Red Light Therapy — What the Research Actually Shows

The evidence is real, the mechanism is well understood, and the marketing has outrun both. A clinician's guide to what photobiomodulation does, how it does it, and what a legitimate device actually looks like.

Dr Kynan Nahrung M.D., J.D. (Hons), BCom, BSc, BMedSci

Clinical Research · 15 July 2026

Red light therapy — more precisely termed photobiomodulation (PBM) — refers to the therapeutic application of red and near-infrared (NIR) light, typically in the 600–1000 nm wavelength range, at non-thermal intensities. The biological effects are real, reproducible, and increasingly well characterised in peer-reviewed literature. The problem is that a legitimate body of science has been substantially obscured by a parallel universe of product marketing that attributes effects to RLT that the evidence does not support, or supports only in preliminary animal models. This article is an attempt to separate those two things cleanly — and then explain, in some depth, why the effects that are real actually occur.

Part One — What the Evidence Actually Supports

The following effects have been documented in controlled human clinical trials, replicated across independent research groups, and in several cases supported by biological plausibility grounded in known cellular mechanisms. They represent the defensible core of what red and near-infrared light therapy can do.

What Is Proven

01

Collagen and Elastin Synthesis

The most robustly supported application of RLT in aesthetic medicine is its capacity to stimulate dermal fibroblasts to upregulate collagen and elastin production. A randomised controlled trial by Wunsch and Matuschka demonstrated statistically significant improvements in skin roughness, fine lines, intradermal collagen density, and elasticity following red (611–650 nm) and NIR (570–850 nm) LED treatment twice weekly over 30 sessions.1 Barolet et al. confirmed the mechanism in vitro, demonstrating that pulsed 660 nm LED light directly upregulates procollagen type I and matrix metalloproteinase-9 (MMP-9) in cultured human dermal fibroblasts, providing a cellular-level explanation for the clinical observations.2 Lee et al. conducted a prospective split-face RCT and found significant improvements in skin roughness and collagen content on the treated side, with histological confirmation of increased collagen deposition.3

02

Hair Growth Stimulation

Low-level laser and LED therapy has genuine, replicated evidence for promoting hair growth in androgenetic alopecia. A multicentre, randomised, sham device-controlled double-blind study by Jimenez et al. demonstrated a statistically significant increase in terminal hair density in both male and female pattern hair loss following LLLT treatment with a 655 nm device.4 A systematic review by Avci et al. concluded that LLLT increases hair count, hair density, and hair tensile strength, with results consistent across multiple RCTs, though the magnitude varies by device power, wavelength, and treatment protocol.5 The US FDA has cleared several LLLT devices for hair growth under the 510(k) pathway — a meaningful regulatory marker that requires demonstrated safety and efficacy.5 The mechanism is discussed in Part Two.

03

Wound Healing and Tissue Repair

Multiple controlled trials have shown accelerated wound healing with PBM. A systematic review by Peplow et al. examining 36 studies found that LLLT significantly accelerated wound closure in both acute and chronic wounds, with effects on fibroblast proliferation, angiogenesis, and inflammatory modulation.6 The evidence is stronger for superficial wounds, diabetic ulcers, and post-surgical healing than for deep tissue repair — an important qualification given the depth-of-penetration limits of visible red light.

04

Skeletal Muscle Recovery and Performance

There is credible and replicated evidence that pre-exercise PBM reduces muscle fatigue, delayed onset muscle soreness (DOMS), and markers of exercise-induced oxidative damage. A meta-analysis by Leal Junior et al. examining 22 RCTs found that PBM applied to muscle groups prior to high-intensity exercise significantly reduced creatine kinase levels (a marker of muscle damage), reduced post-exercise soreness, and improved time to exhaustion.7 These effects are mechanistically coherent with the mitochondrial effects described in Part Two.

05

Reduction of Inflammation

PBM has demonstrable anti-inflammatory effects, operating through modulation of reactive oxygen species (ROS), nitric oxide (NO) release, and downstream reduction in pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6.8 These effects have been demonstrated in both in vitro and in vivo human models. They are relevant to the above applications — inflammation suppression contributes to wound healing, muscle recovery, and the fibroblast environment — and likely underpin some of the pain-modulating effects observed clinically.

The evidence base for red light therapy is real — but it is specific. It applies to defined wavelengths, defined irradiances, and defined tissue targets. None of that specificity appears in consumer marketing.

What Is Not Proven — Advertising Claims vs Evidence

The following are claims that appear prominently in consumer marketing for RLT devices and panels. For each, the evidentiary status is materially weaker than the marketing implies — either limited to animal models, derived from small pilot studies without replication, or based on a plausible mechanism being extrapolated into an outcome the evidence has not actually demonstrated in humans.

Osteoarthritis and Joint Repair
The claimRLT repairs cartilage, reverses arthritis, restores joint function
The evidenceMixed and methodologically limited human trials; animal models show cartilage effects not replicated at scale in humans
What we can sayPBM may reduce joint pain and inflammation modestly — but repair of cartilage in established osteoarthritis is not supported by current human evidence9
Vision Improvement and Macular Degeneration
The claimNIR light improves eyesight and reverses age-related macular degeneration
The evidenceA single small pilot RCT (n=14) by Shinhmar et al. showed short-term improvements in colour contrast sensitivity with a 670 nm device — the findings are preliminary and require large-scale replication10
What we can sayMechanistically plausible in theory; not yet demonstrated in adequately powered human trials; direct ocular exposure to high-intensity devices carries risk10
Testosterone and Hormone Optimisation
The claimGenital or testicular RLT raises testosterone levels
The evidenceOne Iranian study in subfertile men showed some improvement in sperm parameters; the extrapolation to testosterone elevation in healthy men is not evidence-based11
What we can sayNot demonstrated in controlled human trials; the claim substantially outruns the data
Fat Loss and Body Composition
The claimRLT dissolves fat and reshapes body composition
The evidenceSome trials show transient reduction in waist circumference, but effect sizes are small, mechanisms are poorly characterised, and results are not replicated in high-quality RCTs11
What we can sayNot an established fat-loss modality; energy balance and resistance training remain the only reliably evidence-based tools
Cognitive Enhancement and Depression
The claimTranscranial NIR improves cognition, memory, and treats depression
The evidenceSmall pilot studies show some signals in traumatic brain injury and major depressive disorder — but the trials are small, methodologically heterogeneous, and preliminary12
What we can sayMechanistically interesting; does not yet meet the evidentiary bar for clinical recommendation; penetration of NIR through the skull to cortical tissue is also physically limited12

The pattern across unsubstantiated claims is consistent: a plausible cellular mechanism (usually mitochondrial) is identified in vitro or in animal models, then marketed directly to consumers as a clinical outcome without the intervening step of adequately powered human RCTs. The mechanism may well be real. The leap from mechanism to clinical benefit in humans at the parameters achievable by a consumer device is not.

Part Two — How It Actually Works

The Primary Photoreceptor: Cytochrome c Oxidase

The mechanism of photobiomodulation begins with a specific molecular target: cytochrome c oxidase (CCO), also known as Complex IV of the mitochondrial electron transport chain. CCO contains copper and haem chromophores whose absorption spectra align closely with the therapeutic window of red and NIR light — specifically 630–700 nm and 800–1000 nm.13 This is not coincidence; it is the basis for why those wavelengths produce biological effects while others at the same energy levels do not.

Karu's foundational research established that CCO is the primary photoacceptor in mammalian cells, and that its absorption of photons in the red/NIR range leads to a cascade of downstream signalling events that ultimately increase cellular energy production and reduce oxidative stress.13,14 This has since been confirmed by multiple independent research groups and represents the most robust mechanistic explanation for the observed biological effects of PBM.

The Electron Transport Chain and ATP Production

To understand why light hitting CCO matters, it helps to understand what CCO does. The mitochondrial electron transport chain (ETC) is the final stage of cellular respiration — the process by which cells convert substrates (glucose, fatty acids, amino acids) into adenosine triphosphate (ATP), the universal cellular energy currency.

The ETC consists of four protein complexes (I–IV) embedded in the inner mitochondrial membrane, plus ATP synthase (Complex V). Electrons derived from NADH and FADH₂ pass sequentially through these complexes, releasing energy that is used to pump protons (H⁺) across the inner membrane, creating an electrochemical gradient — the proton motive force — that drives ATP synthesis as protons flow back through ATP synthase.15

Cytochrome c oxidase, as Complex IV, is the terminal electron acceptor: it transfers electrons from cytochrome c to molecular oxygen, reducing it to water. Under normal physiological conditions, CCO operates near maximum capacity. But under conditions of cellular stress — hypoxia, oxidative damage, nitric oxide-mediated inhibition, or the metabolic decline of ageing — CCO activity is suppressed, and ATP production falls below the cell's requirements.13,16

This is where photobiomodulation intervenes. Absorption of red/NIR photons by CCO's chromophores appears to dissociate inhibitory nitric oxide from the enzyme's active site, restoring electron flow and increasing ATP production.16 Additionally, the transient increase in mitochondrial membrane potential following PBM exposure activates downstream signalling — including release of reactive oxygen species as second messengers, activation of transcription factors such as NF-κB and AP-1, and upregulation of growth factors including TGF-β1 and basic FGF.14,17

Photobiomodulation does not add energy to cells — it removes a block on energy production. The distinction matters: in healthy, well-functioning cells, the effect is modest. In stressed, hypoxic, or ageing cells operating below capacity, the effect can be substantial.

How Fibroblasts Respond — The Collagen Connection

Dermal fibroblasts are among the most photosensitive cell types studied. Following PBM exposure, fibroblasts demonstrate increased ATP production, enhanced proliferation, upregulated synthesis of procollagen type I and type III, and increased activity of enzymes involved in extracellular matrix remodelling.2,18 The mechanism runs directly through CCO: increased mitochondrial activity raises intracellular ATP, which provides the energetic substrate for the energetically expensive process of collagen synthesis — each procollagen molecule requires hydroxylation of proline and lysine residues in a reaction that consumes ascorbate and oxygen.2

TGF-β1, upregulated downstream of PBM's ROS signalling, is a potent driver of fibroblast-to-myofibroblast differentiation and collagen gene transcription.17 This provides a second mechanistic pathway, independent of direct ATP effects, by which PBM stimulates collagen deposition. The convergence of these two pathways — bioenergetic and signalling — explains why the collagen effects of PBM are among the most reproducible in the literature.

Mitochondria, Ageing, and Why Their Number Matters

Mitochondria are not simply the cell's power plants — they are dynamic organelles that exist in a constant state of fusion, fission, and turnover, and whose number, morphology, and functional capacity are tightly regulated in response to metabolic demand. Understanding mitochondria in the context of ageing is central to understanding why PBM has particular relevance as an anti-ageing intervention.

Each human cell contains between a few hundred and several thousand mitochondria, depending on the cell's energy requirements. Cells with the highest metabolic demands — cardiomyocytes, neurons, skeletal muscle fibres, and hepatocytes — have the highest mitochondrial density. The process of generating new mitochondria is called mitochondrial biogenesis, and it is primarily regulated by a transcriptional co-activator called PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), which acts as a master regulator of mitochondrial number and oxidative capacity.19

With age, mitochondrial function declines through several converging mechanisms: accumulation of mitochondrial DNA (mtDNA) mutations due to proximity to the ETC's ROS production, progressive decline in mitophagy (the selective autophagy that removes dysfunctional mitochondria), reduced PGC-1α expression and consequent suppression of biogenesis, and increasing mitochondrial membrane potential instability.20,21 The result is a cell that, as it ages, runs on progressively fewer and progressively less efficient mitochondria — and the consequences are measurable: reduced cellular ATP, increased ROS production from dysfunctional complexes, greater susceptibility to apoptosis, and reduced capacity for repair and regeneration.20

In the skin specifically, the consequences of mitochondrial decline are directly visible. Aged dermal fibroblasts show reduced mitochondrial membrane potential, decreased ATP output, and impaired collagen synthesis compared to young fibroblasts — a phenotypic shift that maps precisely onto the clinical appearance of ageing skin.21 Maintaining higher mitochondrial number and function is not merely a theoretical anti-ageing marker — it is increasingly understood as a mechanistic driver of biological age at the cellular level.

Mitochondrial Biogenesis — The Animal Evidence

In animal models, PBM has been shown to do something beyond simply activating existing CCO: it appears to stimulate mitochondrial biogenesis — an increase in the actual number of mitochondria per cell. Ferraresi et al. demonstrated in rodent skeletal muscle that repeated PBM exposure increased the expression of PGC-1α, mitochondrial transcription factor A (TFAM), and cytochrome c synthase (CCS) — all markers of de novo mitochondrial production — alongside measurable increases in mitochondrial density on electron microscopy.22 Subsequent work in the same laboratory showed that these biogenesis markers correlated with functional improvements in exercise capacity and muscle fatigue resistance.22

It is important to be precise about where this evidence stands: these findings are from animal models — predominantly rodent skeletal muscle — and the direct demonstration of PBM-induced mitochondrial biogenesis in human tissue remains to be established through adequately powered trials. The mechanism is plausible, the animal data are consistent, and the downstream functional effects observed in human exercise studies are coherent with it — but the specific claim of increased mitochondrial number in human tissue following PBM exposure has not yet been formally proven at the same level of direct cellular evidence available from animal studies.22,23 This is an area of active research, and the distinction between a biologically plausible and mechanistically supported hypothesis and an established clinical fact matters — even when the hypothesis is compelling.

IR & NIR Light Therapy: Pathway to Collagen & Elastin Production Near-Infrared (NIR) Infrared / Thermal (IR) NIR light, 700–1200 nm Non-thermal, photobiomodulation IR (far-infrared) heat >1200 nm, mild hyperthermia Absorbed by cytochrome c oxidase Mitochondrial Complex IV Tissue warms 1–3°C Local mild hyperthermia Displaces inhibitory nitric oxide Unblocks electron transport chain Heat-shock response triggered HSP47 + vasodilation ATP surge + ROS burst Secondary messengers Increased blood flow & oxygen Nutrient delivery to fibroblasts Signalling cascades activated NF-κB, MAPK/ERK, TGF-β/Smad Fibroblast activation & proliferation Increased migration Collagen & elastin genes turned on COL1A1, COL3A1, ELN Collagen & elastin synthesized Secreted into the ECM Collagen breakdown reduced Lower MMP expression Net effect Firmer, smoother, more elastic skin
Mechanism of action of red and near-infrared light therapy on hair growth Flowchart showing red and NIR light absorbed by the scalp, taken up by cytochrome c oxidase in follicle mitochondria and also triggering local nitric oxide release and vasodilation. These converge to activate signaling cascades (NF-kB, MAPK/ERK, Wnt/beta-catenin), activating dermal papilla and bulge stem cells, shifting follicles from telogen to anagen phase, upregulating growth factors (VEGF, FGF7/KGF, IGF-1) and reducing local DHT via lower 5-alpha-reductase activity, resulting in a longer anagen phase and thicker, denser hair. Red & NIR Light Therapy: Pathway to Hair Growth Red & NIR light applied to scalp 630–670 nm and 800–900 nm Absorbed by cytochrome c oxidase Follicle mitochondria, Complex IV Nitric oxide released locally Diffuses into microvasculature Displaces inhibitory nitric oxide Unblocks electron transport chain Local vasodilation occurs Increased blood flow to follicle ATP surge + ROS burst Secondary messengers More oxygen & nutrients delivered Fuels follicle metabolism Signalling cascades activated NF-κB, MAPK/ERK, Wnt/β-catenin Dermal papilla cells activated Bulge stem cells engaged Follicle shifts telogen to anagen Resting to active growth phase Growth factors upregulated VEGF, FGF7/KGF, IGF-1 Local DHT reduced Lower 5-alpha-reductase activity Net effect Longer anagen phase, thicker, denser hair

Part Three — What to Look For in a Device

The consumer RLT market is saturated with devices that vary by several orders of magnitude in actual therapeutic output. A device that glows red is not necessarily delivering photobiomodulation at a clinically relevant dose — and most consumer-grade products do not disclose the parameters required to evaluate whether they do. The following are the specifications that matter.

Irradiance — The Parameter That Matters Most

Irradiance (power density) is expressed in milliwatts per square centimetre (mW/cm²) and describes the amount of light energy delivered to a unit area of tissue per unit time. It is the single most important parameter for determining whether a device is capable of producing biological effects — and it is the parameter most consistently omitted from consumer device marketing.

The published literature on PBM efficacy clusters around irradiances of 10–100 mW/cm² at the treatment surface, with most positive clinical trial results falling in the 30–100 mW/cm² range at the prescribed treatment distance.24 Below approximately 10 mW/cm² at the skin surface, the evidence for meaningful biological effect becomes thin; above approximately 200 mW/cm², thermal effects begin to emerge and the distinction between PBM and thermal laser therapy blurs.

The critical practical implication is that irradiance falls rapidly with distance — following an inverse square law for point sources, and more gradually but still substantially for LED panels. A device that delivers 100 mW/cm² at 5 cm may deliver only 25–35 mW/cm² at 20 cm. The relevant specification is therefore irradiance at the treatment distance you will actually use — not the device's surface irradiance, which is the figure most commonly quoted by manufacturers.24,25

For practical purposes, a minimum of approximately 80 mW/cm² at a treatment distance of 20 cm is a reasonable threshold for a device intended to produce the effects documented in the clinical literature. Devices that cannot demonstrate this specification through independent measurement — not manufacturer claims — should be regarded sceptically. Several independent testing services (including peer-reviewed measurement studies) have documented that many commercial devices deliver substantially less than their advertised specifications, particularly at treatment distances beyond 10 cm.25

Wavelengths — Which Matter and Why

Not all wavelengths in the red and NIR range are equally effective, and the absorption spectrum of cytochrome c oxidase defines which wavelengths are likely to produce meaningful biological effects. The published absorption peaks of CCO's copper and haem chromophores fall in two primary windows: approximately 630–680 nm (visible red) and 800–870 nm (near-infrared), with a secondary NIR window extending to approximately 980–1000 nm.13,26

630–680 nm

Visible Red

The most studied red wavelengths — 630 nm, 633 nm, and 660 nm — have the strongest evidence base for superficial tissue effects including dermal fibroblast stimulation, collagen synthesis, and surface wound healing. Red light penetrates approximately 5–10 mm into tissue. The 660 nm wavelength aligns closely with a CCO absorption peak and appears in the majority of positive skin rejuvenation and wound healing trials.1,2,3

800–870 nm

Near-Infrared

NIR wavelengths penetrate significantly deeper — up to 20–40 mm in some tissue types — making them more relevant for musculoskeletal applications, hair follicle stimulation (follicles sit in the deep dermis and upper subcutis), and any indication where the target tissue lies below the superficial dermis. The most studied wavelengths are 810 nm, 830 nm, and 850 nm. The 810 nm wavelength in particular appears in a high proportion of positive LLLT hair growth and muscle recovery trials.4,5,7

940–1000 nm

Far Near-Infrared

Wavelengths at the longer end of the NIR range — 940 nm and 1000 nm — have demonstrated effects in both in vitro models and some clinical trials, though the evidence base is less extensive than for the 810–850 nm range. They offer deep tissue penetration and may have particular relevance for applications targeting deeper anatomical structures. Some commercially available devices include these wavelengths in combination with the core red and NIR bands.26

Outside 600–1000 nm

Wavelengths to Be Cautious About

Wavelengths below 600 nm are absorbed preferentially by melanin and haemoglobin rather than CCO, limiting their penetration and photobiomodulatory effect. Wavelengths above approximately 1100 nm are absorbed by water in tissue, producing heat rather than photobiomodulation. Devices that advertise primarily blue, green, or UV wavelengths for the effects attributed in the PBM literature are not operating through the established cytochrome c oxidase mechanism.13

Combination Wavelength Devices

Most quality clinical-grade devices now combine red (630–660 nm) and NIR (810–850 nm) wavelengths in a single panel — a pragmatic choice that delivers both superficial and deep tissue effects simultaneously. The combination is supported by the literature: the two wavelength windows target different CCO absorption peaks and likely act synergistically rather than redundantly.26 When evaluating a combination device, the relevant question is whether each wavelength band independently meets the irradiance threshold at treatment distance — not whether the combined total output is impressive on paper.

Treatment Duration and Dose

Photobiomodulation follows a biphasic dose-response curve — meaning that both insufficient and excessive dose produce suboptimal outcomes, with a therapeutic window in between.27 The concept of optical dosing (fluence, measured in J/cm²) integrates irradiance with time: a device delivering 80 mW/cm² for 10 minutes delivers 48 J/cm². Most positive clinical trials for skin rejuvenation and wound healing used fluences in the range of 4–60 J/cm² per session, with session frequencies of three to five times per week for 4–12 weeks.1,3,24 Longer sessions with very high irradiance devices do not necessarily produce proportionally greater effects and may in some contexts suppress the biological response — an important point for those inclined to treat the dose-response curve as linear.

A device specification sheet should show you: irradiance at 20 cm (not at the LEDs), the specific wavelengths emitted (not a range), and ideally independent third-party measurement data. If none of those three things are provided, the device is not being sold on its clinical merits.

References

  1. Wunsch A, Matuschka K. A controlled trial to determine the efficacy of red and near-infrared light treatment in patient satisfaction, reduction of fine lines, wrinkles, skin roughness, and intradermal collagen density increase. Photomed Laser Surg. 2014;32(2):93–100.
  2. Barolet D, Roberge CJ, Auger FA, Boucher A, Germain L. Regulation of skin collagen metabolism in vitro using a pulsed 660 nm LED light source: clinical correlation with a single-blinded randomized clinical study. J Invest Dermatol. 2009;129(12):2751–2759.
  3. Lee SY, Park KH, Choi JW, et al. A prospective, randomized, placebo-controlled, double-blinded, and split-face clinical study on LED phototherapy for skin rejuvenation: clinical, profilometric, histologic, ultrastructural, and biochemical evaluations and comparison of three different treatment settings. J Photochem Photobiol B. 2007;88(1):51–67.
  4. Jimenez JJ, Wikramanayake TC, Bergfeld W, et al. Efficacy and safety of a low-level laser device in the treatment of male and female pattern hair loss: a multicenter, randomized, sham device–controlled, double-blind study. Am J Clin Dermatol. 2014;15(2):115–127.
  5. Avci P, Gupta GK, Clark J, Wikonkal N, Hamblin MR. Low-level laser (light) therapy (LLLT) for treatment of hair loss. Lasers Surg Med. 2014;46(2):144–151.
  6. Peplow PV, Chung TY, Baxter GD. Laser photobiomodulation of wound healing: a review of experimental studies in mouse and rat animal models. Photomed Laser Surg. 2010;28(3):291–325.
  7. Leal Junior EC, Lopes-Martins RA, Frigo L, et al. Effects of low-level laser therapy (LLLT) in the development of exercise-induced skeletal muscle fatigue and changes in biochemical markers related to postexercise recovery. J Orthop Sports Phys Ther. 2010;40(8):524–532.
  8. Hamblin MR. Mechanisms and mitochondrial redox signaling in photobiomodulation. Photochem Photobiol. 2018;94(2):199–212.
  9. Bjordal JM, Johnson MI, Lopes-Martins RA, Bogen B, Chow R, Ljunggren AE. Short-term efficacy of physical interventions in osteoarthritic knee pain: a systematic review and meta-analysis of randomised placebo-controlled trials. BMC Musculoskelet Disord. 2007;8:51.
  10. Shinhmar H, Grewal M, Sarkar S, et al. Optically improved mitochondrial function redeems aged human visual decline. J Gerontol A Biol Sci Med Sci. 2020;75(9):e49–e52.
  11. Avci P, Nyame TT, Gupta GK, Sadasivam M, Hamblin MR. Low-level laser therapy for fat layer reduction: a comprehensive review. Lasers Surg Med. 2013;45(6):349–357.
  12. Cassano P, Petrie SR, Hamblin MR, Henderson TA, Iosifescu DV. Review of transcranial photobiomodulation for major depressive disorder: targeting brain metabolism, inflammation, oxidative stress, and neurogenesis. Neurophotonics. 2016;3(3):031404.
  13. Karu TI. Mitochondrial signaling in mammalian cells activated by red and near-IR radiation. Photochem Photobiol. 2008;84(5):1091–1099.
  14. Chung H, Dai T, Sharma SK, Huang YY, Carroll JD, Hamblin MR. The nuts and bolts of low-level laser (light) therapy. Ann Biomed Eng. 2012;40(2):516–533.
  15. Mitchell P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature. 1961;191:144–148.
  16. Lane N. Cell biology: power games. Nature. 2006;443(7114):901–903.
  17. Chen AC, Arany PR, Huang YY, et al. Low-level laser therapy activates NF-kB via generation of reactive oxygen species in mouse embryonic fibroblasts. PLoS One. 2011;6(7):e22453.
  18. Houreld NN, Masha RT, Abrahamse H. Low-intensity laser irradiation at 660 nm stimulates cytochrome c oxidase in stressed fibroblast cells. Lasers Surg Med. 2012;44(5):429–434.
  19. Scarpulla RC. Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network. Biochim Biophys Acta. 2011;1813(7):1269–1278.
  20. López-Lluch G, Irusta PM, Navas P, de Cabo R. Mitochondrial biogenesis and healthy aging. Exp Gerontol. 2008;43(9):813–819.
  21. Krutmann J, Schroeder P. Role of mitochondria in photoaging of human skin: the defective powerhouse model. J Investig Dermatol Symp Proc. 2009;14(1):44–49.
  22. Ferraresi C, Huang YY, Hamblin MR. Photobiomodulation in human muscle tissue: an advantage in sports performance? J Biophotonics. 2016;9(11–12):1273–1299.
  23. De Marchi T, Leal Junior EC, Bortoli C, Tomazoni SS, Lopes-Martins RA, Salvador M. Low-level laser therapy (LLLT) in human progressive-intensity running: effects on exercise performance, skeletal muscle status, and oxidative stress. Lasers Med Sci. 2012;27(1):231–236.
  24. Hamblin MR. Photobiomodulation for Alzheimer's disease: has the light dawned? Photonics. 2019;6(3):77.
  25. Carroll JD, Milward MR, Cooper PR, Hadis M, Palin WM. Developments in low level light therapy (LLLT) for dentistry. Dent Mater. 2014;30(5):465–475.
  26. Hamblin MR. Mechanisms and applications of the anti-inflammatory effects of photobiomodulation. AIMS Biophys. 2017;4(3):337–361.
  27. Huang YY, Sharma SK, Carroll J, Hamblin MR. Biphasic dose response in low level light therapy — an update. Dose Response. 2011;9(4):602–618.
This article is intended for general informational and educational purposes and does not constitute medical advice. Always consult a registered medical practitioner before commencing any treatment. References are provided above.
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