Peripheral Artery Disease and NAD+: Mitochondrial Health, Vascular Aging, and Emerging Clinical Evidence

Key Takeaways

• PAD goes beyond leg pain: Peripheral artery disease (PAD) is a condition linked to accelerated vascular aging, mitochondrial dysfunction, and oxidative stress.
• NAD+ supports vascular and cellular health: NAD+ levels decline with age, affecting energy production, responses to oxidative stress, and endothelial function.
• Increasing NAD+ shows promise in PAD: Early clinical NR studies suggest improvements in walking performance, vascular function, and cognition.
• NAD+ precursors may have disease-modifying potential: Increasing NAD+ levels could help target underlying cellular mechanisms, not just symptoms.
• More research is needed: Larger, controlled studies are required to confirm benefits, dosing, and patient selection.

For millions of people, leg pain or cramping isn’t just a mild annoyance—it can sometimes signal a serious condition called peripheral artery disease (PAD). Affecting over 200 million people worldwide and 12 million in the United States, PAD is a common age-related vascular disease associated with cardiovascular complications. It can drastically impair quality of life and, in advanced stages, can lead to challenges like limb ischemia (a critical reduction in blood flow to the limbs), amputation, heart attack, stroke, and premature death.

PAD develops when atherosclerotic plaque accumulates in the arteries supplying the limbs—most commonly the legs—which restricts blood flow and limits the delivery of oxygen and nutrients to skeletal muscle, peripheral nerves, and skin. Early symptoms may be subtle or even absent, but as PAD progresses, people may experience intermittent claudication (leg pain with walking), leg numbness or weakness, reduced exercise capacity, impaired wound healing, and, in severe cases, limb-threatening ischemia.

Increasingly, PAD is being studied in the context of accelerated vascular aging. As we grow older, arteries undergo structural and functional changes, including low-grade inflammation, increased oxidative stress, endothelial dysfunction, and declining mitochondrial function.¹ These age-related changes reduce vascular resilience, impair circulation, and contribute not only to PAD but to cardiovascular disease more broadly.

Current treatments primarily focus on managing symptoms and cardiovascular risk, rather than addressing these underlying cellular drivers of vascular aging. Therefore, researchers have a growing interest in strategies that target these mechanisms—like nicotinamide adenine dinucleotide (NAD+), an essential coenzyme involved in cellular energy production and mitochondrial function whose levels decline with age.

NAD+ precursor compounds—including nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (NAM), and niacin—are being studied for their ability to restore NAD+ levels and support vascular health. Notably, the clinical studies conducted specifically in individuals with PAD to date have examined NR as one approach to restoring NAD+ levels.²'³

In this article, we’ll explore PAD through the lens of mitochondrial health and vascular aging, including reviewing its pathophysiology, the rationale for targeting NAD+ in vascular dysfunction, and the emerging clinical evidence, highlighting two recent studies that look at NR supplementation in individuals with PAD.

What Is Peripheral Artery Disease? Symptoms, Risk Factors, and Current Treatments

Peripheral artery disease (PAD) develops when atherosclerotic plaques—the same plaques that contribute to heart attacks and strokes—narrow the arteries, restricting blood flow to the extremities. 

Many people with PAD are initially asymptomatic or notice only mild changes, such as cramping, fatigue, or a cold sensation in the legs. However, as the disease progresses, symptoms can develop into intermittent claudication—leg pain or discomfort that occurs during activity and resolves with rest. While intermittent claudication may seem minor, it can reduce mobility, limit participation in daily activities, and interfere with social engagement, creating a downward spiral of inactivity and deconditioning.⁴  

In some cases, PAD can advance to critical limb ischemia, also known as chronic limb-threatening ischemia (CLTI)—a severe blockage in the arteries of the lower extremities.⁵ This can cause persistent pain in the legs or toes, even at rest, and if left untreated, may result in amputation. 

Although PAD primarily affects the legs, it is not confined to the lower extremities. The disease reflects systemic endothelial and vascular dysfunction, making it a marker for broader cardiovascular risk⁶ and elevated mortality⁷—especially in older adults.

Traditional risk factors for PAD include age over 65, male sex, smoking, high blood pressure, high cholesterol, obesity, family history of cardiovascular disease, and a sedentary lifestyle. Current treatment approaches typically focus on lifestyle modifications (such as quitting smoking), exercise therapy, medications to improve circulation or reduce cardiovascular risk, or surgical procedures.

At the root of PAD is an underlying dysfunction on a cellular level. Oxidative stress, mitochondrial impairment, and reduced cellular energy production can contribute to the vascular and tissue changes seen in PAD, highlighting the importance of interventions that address these foundational mechanisms.⁸

The Cellular Dysfunction Behind Peripheral Artery Disease: Oxidative Stress and Mitochondrial Impairment

PAD represents profound cellular dysfunction that goes well beyond the visible narrowing of arteries. At its core, the disease involves oxidative stress, mitochondrial dysfunction, and muscle fiber damage.

Oxidative stress occurs when reactive oxygen species (ROS)—highly reactive molecules generated during metabolism—accumulate faster than the body can neutralize them.⁹ Excessive ROS accumulation can damage proteins, lipids, and DNA throughout the body, including the endothelial cells that line blood vessels.¹⁰ Endothelial oxidative damage can lead to impaired nitric oxide production.¹¹ Nitric oxide is a beneficial molecule that regulates blood flow, vascular dilation, and blood vessel health, so reduced levels can contribute to poor circulation and tissue oxygenation in the limbs.¹²

At the same time, PAD is also characterized by mitochondrial dysfunction.⁸ As the powerhouses of the cells, mitochondria are vital for producing cellular energy in the form of ATP, a process that depends on adequate oxygen supply. Because oxygen delivery relies on healthy blood flow, restricted blood flow in people with PAD limits oxygen availability to skeletal muscle. Combined with impaired mitochondrial function, this restriction reduces ATP production and creates a cellular energy deficit—contributing to muscle weakness, fatigue, and tissue damage.⁸

Importantly, the consequences of these cellular changes extend beyond the legs, affecting multiple organ systems. In addition to skeletal muscle damage, those with PAD may experience functional decline,6 mobility loss,6 cognitive impairment,¹³ and fatigue. 

Together, oxidative stress, mitochondrial dysfunction, and impaired cellular energy production are all interconnected in PAD. Recognizing this interconnected biology highlights the potential value of targeted interventions, such as NAD+ restoration, aimed at supporting mitochondrial health and cellular resilience to potentially slow disease progression.

NAD+: A Master Regulator of Cellular Energy, Repair, and Mitochondrial Health

Nicotinamide adenine dinucleotide (NAD+) is a fundamental coenzyme present in every living cell, playing a central role in energy metabolism, cellular repair, and mitochondrial health.¹⁴ Within the mitochondria, NAD+ acts as an electron carrier, facilitating the conversion of nutrients into ATP, which cells rely on to maintain normal function.¹⁴

NAD+ is essential for the processes that are disrupted in PAD, including vascular function,¹⁵ mitochondrial health,¹⁶ and oxidative stress responses.¹⁷ Two families of NAD-dependent enzymes are critical to these processes, including poly(ADP-ribose) polymerases (PARPs) and sirtuins. 

Sirtuins, especially SIRT1, regulate cellular health, stress responses, and longevity, in addition to supporting vascular health and nitric oxide production.¹⁸ PARPs also consume NAD+ to maintain and repair DNA.¹⁹ The activity of sirtuins and PARPs highlights a delicate balance between energy production and repair processes, as when NAD+ is limited, cells have to prioritize between generating energy and DNA maintenance. 

NAD+ levels naturally decline with age, a process observed in healthy aging²⁰ and accelerated in certain disease states, such as heart failure.²¹ This decline can be worsened by oxidative stress and DNA damage, which increase PARP activity and deplete NAD+ stores. Endothelial cells are especially vulnerable due to their high metabolic demands and dependence on robust mitochondrial function.²² Reduced NAD+ availability in endothelial cells can impair nitric oxide production, increase oxidative stress, and compromise stress responses—mechanisms that are also central to PAD pathology.²³

While there is currently no direct evidence showing that NAD+ is depleted in PAD patients, the underlying molecular processes tied to low NAD+—like mitochondrial dysfunction, oxidative stress, and impaired vascular health—overlap with key features of the disease. 

This provides a theoretical rationale for NAD+ restoration as a potential therapeutic strategy for PAD, aimed at supporting cellular energy production, enhancing mitochondrial function, and maintaining vascular health. However, personalized approaches are important, as individual responses may vary depending on disease stage, metabolic status, and other factors.

The Potential Connection Between NAD+ and Peripheral Artery Disease

Given its central role in mitochondrial function, oxidative stress regulation, and cellular metabolism—all processes disrupted in PAD—NAD+ biology provides a systems-level framework for understanding the disease. Rather than targeting a single downstream symptom, NAD+ restoration represents an approach aimed at supporting multiple interconnected cellular pathways simultaneously. 

Increasing NAD+ availability may help rebalance cellular energy production, enhance stress resistance, and support repair processes in both vascular endothelial cells and skeletal muscle.²⁴⁻²⁶ These effects align directly with the dysfunction associated with PAD: impaired nitric oxide signaling, mitochondrial dysfunction, oxidative stress, and reduced metabolic resilience.

In human studies, NAD+ restoration is primarily achieved through supplementation with NAD+ precursors, such as NR, NMN, or NAM. Clinical studies have demonstrated that NAD+ levels can be safely and effectively increased in older adults²⁷ and individuals with cardiometabolic or vascular risk.²⁸ Notably, depleted NAD+ levels have been reported in people with certain cardiovascular conditions, including heart failure.²⁹ In patients with this condition, NAD+ elevation has been associated with improvements in markers of mitochondrial health.²⁸ 

Beyond heart failure, studies have observed trends toward improved arterial stiffness³⁰ and blood pressure²⁷ following NR supplementation. While these effects haven’t been tested in PAD specifically, they are relevant given the disease’s characteristic vascular dysfunction and elevated cardiovascular risk.

While direct evidence linking NAD+ with PAD remains limited, these broader vascular and mitochondrial findings provide a strong scientific rationale for investigating NAD-targeted strategies in this population.

Clinical Evidence: NAD+ Supplementation in Peripheral Artery Disease

Two notable clinical studies have directly assessed the use of NAD+ precursors in people with PAD, particularly NR. While these studies differed in design, duration, and measured outcomes, together they provide complementary insights into how NAD+ restoration may influence functional performance and vascular health in PAD populations. 

The most rigorous study to date, published by McDermott et al., was a randomized, double-blind, placebo-controlled trial that enrolled 90 participants with lower extremity PAD.² Over six months, the researchers tested oral NR supplementation—both alone and combined with resveratrol—against a placebo to assess its effects on six-minute walking performance, a clinically meaningful measure of functional capacity in PAD.

Participants receiving NR improved their walking distance by 7.0 meters, while those on placebo declined by 10.6 meters, yielding a between-group difference of 17.6 meters (approximately 58 feet). 

While 17.6 meters may seem modest, walking performance in PAD generally worsens over time. The improvement in the NR group, compared to the decline in the placebo group, makes this difference clinically meaningful.

The effects were even more pronounced among those who took at least 75% of their assigned study pills. In this subgroup, those receiving NR improved their six-minute walk distance by 31.0 meters (over 101 feet), compared to placebo, while those receiving NR combined with resveratrol improved by 26.9 meters. Notably, adding resveratrol did not enhance the effect beyond NR alone.

As lead study author Dr. Mary McDermott noted:

"These results are significant because few therapies have been identified to improve walking impairment in people with peripheral artery disease."

She also observed that, in adherent participants, the magnitude of improvement was comparable to that seen with supervised exercise programs in previous studies.

These benefits were maintained over the six months of NR supplementation, suggesting a persistence of effect rather than just a short-term response. Interestingly, these improvements occurred without changes in ankle-brachial index, meaning that the improvements were likely not due to increased large-vessel blood flow. Instead, these findings support the theory that NR improves cellular and mitochondrial function within skeletal muscle, enhancing walking performance through metabolic rather than structural vascular mechanisms.

A second, smaller study by Szarvas et al.³ looked at NAD+ restoration in PAD patients from a slightly different angle. This pilot trial involved just eight PAD participants who received NR for four weeks. Although the study lacked a control group and was limited in size, it explored outcomes beyond walking performance, examining measures of vascular function, functional cerebrovascular responses, and cognitive performance, reflecting the idea that PAD is a systemic disease. 

After NR supplementation, participants showed promising trends in peripheral endothelial function—the ability of blood vessel linings to regulate blood flow, inflammation, and clotting. They also demonstrated improved cerebrovascular responsiveness, particularly in the left dorsolateral prefrontal cortex, a brain region critical for executive functions like working memory and cognitive flexibility. Cognitive testing also revealed enhancements across multiple domains, suggesting that NR may support brain health in addition to vascular and muscular function in people with PAD.

To better understand some of the underlying mechanisms, the research team treated cultured cerebromicrovascular endothelial cells to blood samples collected from participants after supplementation. The cells showed trends towards lower levels of oxidative stress, increased nitric oxide production, and enhanced mitochondrial efficiency. These findings suggest that NR may enhance endothelial function and energy production at the cellular level.

Although preliminary, these findings suggest that NR supplementation may help address the systemic vascular and cognitive consequences of PAD by improving endothelial function, mitochondrial health, and reducing oxidative stress. Importantly, this study highlights how targeting NAD+, a central metabolic molecule, can produce multiple benefits through shared cellular pathways. Rather than simply easing symptoms, restoring NAD+ levels may influence underlying disease processes, raising the possibility that NR could serve as a disease-modifying strategy.

Taken together, these studies offer early but compelling evidence that NAD+ restoration with NR may benefit people with PAD on multiple levels, from improved walking performance to better vascular and cognitive health. While the sample sizes are small, the consistent pattern of improved mitochondrial efficiency and cellular function suggests a potential biological mechanism. However, larger, well-controlled studies are needed to confirm these findings and clarify the long-term impact of NAD+ restoration in PAD.

Conclusion: NAD+ Restoration as an Area of Active Investigation in Vascular Health

At its core, PAD is characterized by accelerated vascular aging and driven by mitochondrial dysfunction, oxidative stress, and impaired cellular energy production. Thus, NAD+ restoration remains an active area of investigation for its potential to modulate the cellular mechanisms that contribute to PAD.

The early evidence from two clinical studies on NR and PAD showed that, following NR supplementation, participants had improved walking distance, vascular function, and cognitive performance, with trending reductions in oxidative stress, boosted mitochondrial efficiency, and improved nitric oxide production. These findings point to a broader possibility: restoring NAD+ may influence the cellular processes associated with PAD. 

While the results are preliminary and the studies have small sample sizes, they both highlight the role of mitochondrial and cellular health in PAD, offering a clear rationale for future research. If larger trials confirm these results, NAD+ enhancement through precursors like NR may become a complementary strategy alongside current PAD treatments.

Ultimately, NAD+ restoration represents a shift toward targeting the fundamental biology behind vascular aging, offering a new perspective for future investigation on age-related vascular diseases. 

References

1. Ahmed, B., Rahman, A. A., Lee, S., & Malhotra, R. (2024). The Implications of Aging on Vascular Health. International Journal of Molecular Sciences, 25(20), 11188. https://doi.org/10.3390/ijms252011188
2. McDermott, M. M., Martens, C. R., Domanchuk, K. J., Zhang, D., Peek, C. B., Criqui, M. H., Ferrucci, L., Greenland, P., Guralnik, J. M., Ho, K. J., Kibbe, M. R., Kosmac, K., Lloyd-Jones, D., Peterson, C. A., Sufit, R., Tian, L., Wohlgemuth, S., Zhao, L., Zhu, P., & Leeuwenburgh, C. (2024). Nicotinamide riboside for peripheral artery disease: the NICE randomized clinical trial. Nature Communications, 15(1), 5046. https://doi.org/10.1038/s41467-024-49092-5
3. Szarvas, Z., Reyff, Z. A., Peterfi, A., Pinto, C. B., Owens, C. D., Kaposzta, Z., Mukli, P., Pinaffi-Langley, A. C. da C., Adams, C. A., Muranyi, M., Palacios, F. S., Hawkins, B., Baur, J. A., Velez, F. S., Prodan, C. I., Kirkpatrick, A. C., Csiszar, A., Ungvari, Z., Balasubramanian, P., … Yabluchanskiy, A. (2025). Effects of NAD+ supplementation with oral nicotinamide riboside on vascular health and cognitive function in older adults with peripheral artery disease: Results from a pilot 4-week open-label clinical trial. The Journal of Pharmacology and Experimental Therapeutics, 392(7), 103607. https://doi.org/10.1016/j.jpet.2025.103607
4. Egberg, L., Andreassen, S., & Mattiasson, A.-C. (2012). Experiences of living with intermittent claudication. Journal of Vascular Nursing, 30(1), 5–10. https://doi.org/10.1016/j.jvn.2011.11.001
5. Uccioli, L., Meloni, M., Izzo, V., Giurato, L., Merolla, S., & Gandini, R. (2018). Critical limb ischemia: current challenges and future prospects. Vascular Health and Risk Management, 14(0), 63–74. https://doi.org/10.2147/vhrm.s125065
6. Arya, S., Khakharia, A., Rothenberg, K. A., Johnson, T. M., Sawyer, P., Kennedy, R. E., Brown, C. J., & Bowling, C. B. (2020). Association of peripheral artery disease with life-space mobility restriction and mortality in community-dwelling older adults. Journal of Vascular Surgery, 71(6), 2098-2106.e1. https://doi.org/10.1016/j.jvs.2019.08.276
7. Matsushita, K., Gao, Y., Sang, Y., Ballew, S. H., Salameh, M., Allison, M., Selvin, E., & Coresh, J. (2022). Comparative mortality according to peripheral artery disease and coronary heart disease/stroke in the United States. Atherosclerosis, 354, 57–62. https://doi.org/10.1016/j.atherosclerosis.2022.04.029
8. Gratl, A., Wipper, S., Frese, J. P., Raude, B., Greiner, A., & Pesta, D. (2021). The Role of Mitochondrial Function in Peripheral Arterial Disease: Insights from Translational Studies. International Journal of Molecular Sciences, 22(16), 8478. https://doi.org/10.3390/ijms22168478
9. Pizzino, G., Irrera, N., Cucinotta, M., Pallio, G., Mannino, F., Arcoraci, V., Squadrito, F., Altavilla, D., & Bitto, A. (2017). Oxidative Stress: Harms and Benefits for Human Health. Oxidative Medicine and Cellular Longevity, 2017(1), 8416763. https://doi.org/10.1155/2017/8416763
10. Signorelli, S. S., Scuto, S., Marino, E., Xourafa, A., & Gaudio, A. (2019). Oxidative Stress in Peripheral Arterial Disease (PAD) Mechanism and Biomarkers. Antioxidants, 8(9), 367. https://doi.org/10.3390/antiox8090367
11. Förstermann, U. (2010). Nitric oxide and oxidative stress in vascular disease. Pflügers Archiv - European Journal of Physiology, 459(6), 923–939. https://doi.org/10.1007/s00424-010-0808-2
12. Allen, J. D., Giordano, T., & Kevil, C. G. (2012). Nitrite and nitric oxide metabolism in peripheral artery disease. Nitric Oxide : Biology and Chemistry, 26(4), 217–222. https://doi.org/10.1016/j.niox.2012.03.003
13. Cheshire, B. L., Messeder, S. J., Pepper, C. J., Beishon, L. C., Sayers, R. D., & Houghton, J. S. (2025). Association of cognitive impairment and peripheral artery disease (PAD): A systematic review. Vascular Medicine, 30(6), 724–739. https://doi.org/10.1177/1358863x251336736
14. Covarrubias, A. J., Perrone, R., Grozio, A., & Verdin, E. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology, 22(2), 119–141. https://doi.org/10.1038/s41580-020-00313-x
15. Abdellatif, M., Bugger, H., Kroemer, G., & Sedej, S. (2022). NAD+ and Vascular Dysfunction: From Mechanisms to Therapeutic Opportunities. Journal of Lipid and Atherosclerosis, 11(2), 111–132. https://doi.org/10.12997/jla.2022.11.2.111
16. Yusri, K., Jose, S., Vermeulen, K. S., Tan, T. C. M., & Sorrentino, V. (2025). The role of NAD+ metabolism and its modulation of mitochondria in aging and disease. Npj Metabolic Health and Disease, 3(1), 26. https://doi.org/10.1038/s44324-025-00067-0
17. Massudi, H., Grant, R., Braidy, N., Guest, J., Farnsworth, B., & Guillemin, G. J. (2012). Age-Associated Changes In Oxidative Stress and NAD+ Metabolism In Human Tissue. PLoS ONE, 7(7), e42357. https://doi.org/10.1371/journal.pone.0042357
18. Chung, S., Yao, H., Caito, S., Hwang, J., Arunachalam, G., & Rahman, I. (2010). Regulation of SIRT1 in cellular functions: Role of polyphenols. Archives of Biochemistry and Biophysics, 501(1), 79–90. https://doi.org/10.1016/j.abb.2010.05.003
19. Sousa, F. G., Matuo, R., Soares, D. G., Escargueil, A. E., Henriques, J. A. P., Larsen, A. K., & Saffi, J. (2012). PARPs and the DNA damage response. Carcinogenesis, 33(8), 1433–1440. https://doi.org/10.1093/carcin/bgs132
20. Massudi, H., Grant, R., Braidy, N., Guest, J., Farnsworth, B., & Guillemin, G. J. (2012). Age-Associated Changes In Oxidative Stress and NAD+ Metabolism In Human Tissue. PLoS ONE, 7(7), e42357. https://doi.org/10.1371/journal.pone.0042357
21. Breton, M., Costemale-Lacoste, J.-F., Li, Z., Lafuente-Lafuente, C., Belmin, J., & Mericskay, M. (2020). Blood NAD levels are reduced in very old patients hospitalized for heart failure. Experimental Gerontology, 139, 111051. https://doi.org/10.1016/j.exger.2020.111051
22. Grossini, E., Venkatesan, S., & Pour, M. M. O. (2025). Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging. Antioxidants, 14(4), 372. https://doi.org/10.3390/antiox14040372
23. Csiszar, A., Tarantini, S., Yabluchanskiy, A., Balasubramanian, P., Kiss, T., Farkas, E., Baur, J. A., & Ungvari, Z. (2019). Role of endothelial NAD+ deficiency in age-related vascular dysfunction. American Journal of Physiology-Heart and Circulatory Physiology, 316(6), H1253–H1266. https://doi.org/10.1152/ajpheart.00039.2019
24. Yang, Y., & Sauve, A. A. (2016). NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics, 1864(12), 1787–1800. https://doi.org/10.1016/j.bbapap.2016.06.014
25. Freeberg, K. A., Ludwig, K. R., Chonchol, M., Seals, D. R., & Rossman, M. J. (2023). NAD+-boosting compounds enhance nitric oxide production and prevent oxidative stress in endothelial cells exposed to plasma from patients with COVID-19. Nitric Oxide, 140, 1–7. https://doi.org/10.1016/j.niox.2023.08.003
26. Xu, Y., & Xiao, W. (2023). NAD+: An old but promising therapeutic agent for skeletal muscle ageing. Ageing Research Reviews, 92, 102106. https://doi.org/10.1016/j.arr.2023.102106
27. Martens, C. R., Denman, B. A., Mazzo, M. R., Armstrong, M. L., Reisdorph, N., McQueen, M. B., Chonchol, M., & Seals, D. R. (2018). Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications, 9(1), 1286. https://doi.org/10.1038/s41467-018-03421-7
28. Zhou, B., Wang, D. D., Qiu, Y., Airhart, S., Liu, Y., Stempien-Otero, A., O’Brien, K. D., & Tian., R. (2020). Boosting NAD Level Suppresses Inflammatory Activation of PBMC in Heart Failure. Journal of Clinical Investigation, 130(11), 6054–6063. https://doi.org/10.1172/jci138538
29. Breton, M., Costemale-Lacoste, J.-F., Li, Z., Lafuente-Lafuente, C., Belmin, J., & Mericskay, M. (2020). Blood NAD levels are reduced in very old patients hospitalized for heart failure. Experimental Gerontology, 139, 111051. https://doi.org/10.1016/j.exger.2020.111051
30. Shoji, M., Kato, H., Koshizaka, M., Kaneko, H., Baba, Y., Ishikawa, T., Teramoto, N., Kinoshita, D., Yamaguchi, A., Maeda, Y., Inaba, Y., Shiko, Y., Ozawa, Y., Bohr, V. A., Maezawa, Y., & Yokote, K. (2025). Nicotinamide Riboside Supplementation Benefits in Patients With Werner Syndrome: A Double‐Blind Randomized Crossover Placebo‐Controlled Trial. Aging Cell, 24(8), e70093. https://doi.org/10.1111/acel.70093