Klotho Protein Research Guide: Anti-Aging, Cognitive Enhancement & Longevity Mechanisms

Last updated: March 2026 | Medically reviewed content | Browse Research Peptides

In Greek mythology, Klotho was one of three Fates who spun the thread of human life. In 1997, a Japanese research team at the University of Texas Southwestern named a newly discovered gene after her — because when they accidentally disrupted it in mice, the animals aged catastrophically. They developed atherosclerosis by 3 weeks, osteoporosis by 5 weeks, emphysema by 7 weeks, and died of multi-organ failure by 8-9 weeks of age. These mice lived one-tenth of a normal mouse lifespan and exhibited virtually every hallmark of human aging compressed into weeks. The gene they lost was Klotho, and its protein product would become one of the most important discoveries in aging biology.

The opposite experiment was equally dramatic. When Klotho was overexpressed in mice — producing 50-100% more protein than normal — lifespan extended by 20-30%, cognitive function improved, and age-related disease was delayed across nearly every organ system. No genetic modification for a single gene has produced more comprehensive anti-aging effects in mammals. If Klotho were a drug, it would be the most prescribed medication in history. The problem has always been getting it into patients.

In 2023, that problem began to crack. Multiple groups demonstrated that a single injection of Klotho protein could reverse cognitive decline in aged mice within hours. The field went from “interesting science” to “viable therapeutic” almost overnight. This article covers the full scope of Klotho research in 2026: the biology, the aging connection, the cognitive effects, and the therapeutic strategies — including peptide-based approaches — being pursued to harness this remarkable protein.

The Klotho Discovery: An Accidental Breakthrough

The discovery of Klotho was serendipitous. Makoto Kuro-o, working in Yoichi Nabeshima’s laboratory at the National Institute of Neuroscience in Tokyo, was studying a line of transgenic mice when they noticed that one line developed a syndrome of rapid aging. The culprit was an insertional mutation that disrupted the promoter of a previously unknown gene on chromosome 13. When this gene was silenced, mice developed a syndrome that recapitulated essentially every feature of human aging — but compressed into weeks rather than decades (Kuro-o et al., 1997, Nature).

The Klotho-Deficient Phenotype

Klotho-deficient mice exhibit:

• Dramatically shortened lifespan (~8-9 weeks vs ~2.5 years for wild-type)
• Atherosclerosis and medial calcification of arteries
• Osteoporosis with reduced bone mineral density
• Pulmonary emphysema
• Skin atrophy and hair loss
• Cognitive impairment and hippocampal degeneration
• Hypogonadism and infertility
• Ectopic calcification (soft tissue calcification)
• Impaired glucose tolerance
• Thymic involution

This comprehensive aging syndrome from disruption of a single gene was unprecedented. No previously known genetic modification produced such a broad, multi-organ accelerated aging phenotype. The finding immediately elevated Klotho to the highest tier of aging-relevant genes.

The Overexpression Experiment

The complementary experiment — overexpressing Klotho — was published in 2005 by Kurosu et al. Transgenic mice carrying extra copies of the Klotho gene, producing approximately 50% more circulating Klotho protein, lived 20-30% longer than wild-type controls. They showed reduced age-related cognitive decline, improved insulin sensitivity, lower oxidative stress, and protection from age-related cardiovascular disease. The lifespan extension was observed in both males and females and was not associated with obvious growth defects or tumor predisposition (Kurosu et al., 2005, Science).

Klotho Biology: Three Forms, Three Functions

Klotho is not a single molecule but a family of three related proteins. The founding member (?-Klotho) is the most studied and is the focus of anti-aging research.

?-Klotho: The Aging Protein

?-Klotho is a 1,012-amino acid type I transmembrane protein primarily expressed in the kidney distal tubules, brain choroid plexus, and parathyroid gland. It exists in two functional forms:

Membrane-bound ?-Klotho: Functions as a co-receptor for fibroblast growth factor 23 (FGF23) by forming a complex with FGF receptors (FGFR1c, FGFR3c, FGFR4). This membrane-bound form is essential for FGF23 signaling, which regulates phosphate homeostasis, vitamin D metabolism, and calcium balance. Without membrane Klotho, FGF23 cannot effectively signal, leading to the hyperphosphatemia and ectopic calcification that characterizes Klotho-deficient mice.

Soluble ?-Klotho (sKlotho): The extracellular domain of membrane Klotho is cleaved by ADAM10 and ADAM17 (metalloproteinase/disintegrin enzymes) and released into blood, CSF, and urine as a soluble hormone-like factor. Soluble Klotho is the form responsible for most of the systemic anti-aging effects. It circulates in blood at concentrations of approximately 500-1000 pg/mL in young adults, declining to 200-400 pg/mL in elderly individuals (Yamazaki et al., 2010; Semba et al., 2011).

Soluble Klotho exerts anti-aging effects through multiple mechanisms:

• Insulin/IGF-1 signaling inhibition: sKlotho suppresses insulin and IGF-1 receptor signaling — the most conserved longevity pathway across species. This reduces mTOR activation and promotes FOXO-mediated stress resistance gene expression.
• Wnt signaling inhibition: sKlotho binds and sequesters Wnt ligands, suppressing Wnt signaling. Excessive Wnt activity promotes stem cell exhaustion, fibrosis, and senescence. By dampening Wnt, Klotho preserves stem cell pools and tissue homeostasis.
• TGF-?1 signaling inhibition: sKlotho suppresses TGF-?1 signaling, reducing fibrosis in kidney, lung, and heart tissue.
• Oxidative stress resistance: sKlotho upregulates manganese superoxide dismutase (MnSOD) and other antioxidant enzymes through FOXO activation, reducing oxidative damage.
• Anti-inflammatory effects: sKlotho inhibits NF-?B signaling and reduces NLRP3 inflammasome activation, directly counteracting inflammaging.

?-Klotho

?-Klotho is a related but distinct protein that functions as a co-receptor for FGF21 and FGF19 (rather than FGF23). It is primarily expressed in liver, adipose tissue, and the brain, where it mediates FGF21 signaling — a hormone with established anti-aging and metabolic benefits. FGF21 overexpression extends mouse lifespan by ~30%, an effect that requires ?-Klotho. While less studied for anti-aging applications than ?-Klotho, ?-Klotho/FGF21 signaling is an important parallel pathway.

?-Klotho

?-Klotho (also called LCTL or Klotho-related protein) is the least characterized family member, expressed primarily in skin and adipose tissue. Its functions are not well understood, and it has not been implicated in aging to the same degree as ?- and ?-Klotho.

The Klotho-Aging Connection: Why Levels Decline and What Happens When They Do

Age-Related Klotho Decline

Circulating soluble Klotho levels decline progressively with age. In a study of 804 adults aged 18-85, plasma sKlotho decreased approximately 50% between ages 25 and 75, with the sharpest decline occurring between ages 40 and 60. CSF Klotho levels show a parallel decline, with concentrations approximately 50% lower in adults over 65 compared to those under 40 (Semba et al., 2011, The Journals of Gerontology Series A).

The causes of age-related Klotho decline include:

• Kidney function decline: The kidney is the primary source of circulating Klotho. Age-related decline in renal function (GFR decreases ~1 mL/min/year after age 30) reduces Klotho production.
• Epigenetic silencing: The Klotho gene promoter becomes hypermethylated with age, reducing transcription. This is one of the specific methylation changes that epigenetic clocks detect as an aging signal.
• Chronic inflammation: Inflammatory cytokines (TNF-?, IL-6) directly suppress Klotho gene expression in kidney tubular cells and choroid plexus — creating a vicious cycle where inflammaging reduces Klotho, and reduced Klotho impairs anti-inflammatory defenses.
• Oxidative stress: Chronic oxidative stress reduces Klotho expression through NF-?B-mediated transcriptional suppression.

Consequences of Klotho Decline

The decline in Klotho mirrors and potentially drives multiple aging hallmarks:

Vascular calcification: Reduced Klotho impairs FGF23 signaling, leading to phosphate retention. Elevated phosphate promotes calcium-phosphate crystal deposition in arterial walls — the molecular basis of age-related arterial stiffness and atherosclerotic calcification. Klotho-deficient mice develop severe arterial calcification indistinguishable from that seen in advanced human aging.

Kidney fibrosis: Without Klotho-mediated TGF-? suppression, progressive kidney fibrosis occurs. Chronic kidney disease (CKD) is both a cause and consequence of Klotho deficiency — CKD reduces Klotho production, and Klotho deficiency accelerates CKD progression. This feedforward loop explains why CKD patients age more rapidly and exhibit a phenotype remarkably similar to Klotho-deficient mice (Hu et al., 2011; Kuro-o, 2019, Nature Reviews Nephrology).

Cognitive decline: CSF Klotho decline correlates with age-related cognitive impairment. Lower CSF Klotho levels predict faster cognitive decline in longitudinal studies, and Klotho-deficient mice show hippocampal degeneration, impaired LTP, and memory deficits.

Klotho and the Brain: The Cognitive Enhancement Discovery

The most exciting development in Klotho research has been the discovery that even a single, acute administration of Klotho protein can dramatically improve cognitive function in aged mice.

The Dubal Lab Breakthrough

Dena Dubal’s laboratory at UC San Francisco has been at the forefront of Klotho-cognition research. In a landmark 2023 study published in Nature, Dubal’s team demonstrated that a single peripheral injection of the ?-Klotho protein fragment (the KL1 domain, the minimal active fragment) improved spatial memory and working memory in aged mice within 4-24 hours. The cognitive enhancement persisted for at least 2 weeks after a single injection (Castner et al., 2023, Nature Aging).

Key findings from this and related studies:

• Rapid onset: Cognitive improvements were measurable within 4 hours of injection — far too fast to be explained by new synapse formation, suggesting an acute neuromodulatory mechanism
• Persistence: Effects lasted 2+ weeks after a single injection, suggesting induction of sustained neuroplasticity changes
• GluN2B mechanism: Klotho treatment enhanced NMDA receptor function specifically through the GluN2B subunit, which is critical for synaptic plasticity and memory formation. GluN2B expression declines with age, and Klotho appears to restore it
• Dose-response: Cognitive enhancement was observed at multiple doses, with the optimal effect at relatively low doses (10 ?g/kg)
• Cross-species validation: In a parallel study, Klotho improved cognitive performance in aged non-human primates (rhesus macaques), strengthening the translational relevance

How Klotho Enhances Cognition

The mechanism by which peripheral Klotho injection improves brain function is partially understood:

1. GluN2B upregulation: Klotho increases GluN2B-containing NMDA receptor expression in hippocampal synapses, enhancing the calcium influx necessary for long-term potentiation (LTP) and memory formation
2. Synaptic plasticity enhancement: Klotho treatment increases levels of GluA1 (an AMPA receptor subunit) in synaptic fractions, indicating enhanced excitatory synaptic strength
3. BDNF-TrkB signaling: Klotho may potentiate BDNF signaling in the hippocampus, though this mechanism is less well characterized
4. Anti-inflammatory effects: By reducing neuroinflammation (microglial activation, inflammatory cytokine production), Klotho creates a neuronal microenvironment more conducive to synaptic plasticity

The BBB Question

A major unresolved question: does circulating Klotho cross the blood-brain barrier, or does it exert cognitive effects through peripheral signaling? At 130 kDa, the full-length soluble Klotho protein is too large for passive BBB transit. However, the active KL1 domain fragment (~65 kDa) may cross through receptor-mediated transcytosis or act at circumventricular organs (brain regions where the BBB is naturally more permeable). Alternatively, peripheral Klotho may modulate brain function indirectly through effects on inflammatory mediators, metabolic signals, or vagal nerve afferents. The answer has major implications for therapeutic delivery strategies.

Klotho, FGF23, and Kidney Aging

The Klotho-FGF23 axis is central to kidney aging and chronic kidney disease (CKD), and kidney disease represents the most clinically advanced application area for Klotho-based therapeutics.

The Phosphate Toxicity Model

Klotho-deficient mice die primarily from phosphate toxicity. Without membrane Klotho, FGF23 cannot signal to its receptors in the kidney, leading to impaired phosphate excretion. Hyperphosphatemia then drives ectopic calcification (calcium-phosphate deposition in blood vessels, heart, kidneys, and soft tissues), oxidative stress, endothelial dysfunction, and accelerated aging. Remarkably, putting Klotho-deficient mice on a low-phosphate diet rescues much of their accelerated aging phenotype, confirming that phosphate toxicity is a central pathogenic mechanism (Kuro-o, 2019, Nature Reviews Nephrology).

The relevance to human aging is striking: CKD patients (who have reduced renal Klotho) develop accelerated vascular calcification, cardiovascular disease, cognitive decline, and sarcopenia — essentially an accelerated aging phenotype that mirrors Klotho-deficient mice. CKD is now recognized as a model of accelerated aging, and Klotho deficiency is proposed as the mechanistic link.

Klotho as a CKD Biomarker and Therapeutic Target

Plasma Klotho levels decline early in CKD — often before GFR drops to the level that defines clinical CKD (< 60 mL/min). This makes Klotho a potential early biomarker for kidney aging. In the Multi-Ethnic Study of Atherosclerosis (MESA), lower plasma Klotho levels independently predicted incident CKD over 10 years of follow-up, even after adjustment for baseline GFR, albuminuria, and traditional risk factors.

Therapeutic Klotho replacement in CKD animal models has shown dramatic benefits: reduced fibrosis, preserved GFR, decreased proteinuria, and reduced vascular calcification. The challenge is delivery — recombinant Klotho protein is large (130 kDa) and expensive to produce, and the optimal route and frequency of administration for CKD patients has not been established.

Cardiovascular Protection: How Klotho Guards the Vasculature

Klotho’s cardiovascular protective effects are among its most clinically relevant properties, given that cardiovascular disease remains the leading cause of death globally.

Anti-Calcification

Klotho prevents vascular calcification through multiple mechanisms: it reduces phosphate-induced osteogenic differentiation of vascular smooth muscle cells (VSMCs), inhibits the Pit-1 phosphate transporter, and promotes FGF23-mediated renal phosphate excretion. In ApoE-knockout mice (a model of atherosclerosis), Klotho overexpression reduced aortic calcification by 60% and improved arterial compliance (Lim et al., 2012; Hu et al., 2015).

Endothelial Protection

Klotho protects endothelial cells from oxidative stress, inflammatory activation, and senescence. In vitro, Klotho treatment of human endothelial cells reduces TNF-?-induced adhesion molecule expression (VCAM-1, ICAM-1), suppresses NF-?B activation, and inhibits monocyte adhesion — the initiating events of atherosclerotic plaque formation. Klotho also stimulates endothelial nitric oxide (NO) production, promoting vasodilation and preventing endothelial dysfunction.

Cardiac Protection

Klotho protects cardiomyocytes from hypertrophic signaling and oxidative damage. Klotho-deficient mice develop cardiac hypertrophy and diastolic dysfunction by 4-6 weeks of age. Conversely, Klotho supplementation in animal models of heart failure reduces cardiac hypertrophy, improves ejection fraction, and reduces fibrosis. The mechanisms involve inhibition of TRPC6 calcium channels, suppression of calcineurin-NFAT signaling, and reduction of oxidative stress through FOXO3a-mediated antioxidant gene induction.

Klotho as a Tumor Suppressor

An important aspect of Klotho biology — and a key differentiator from growth-promoting anti-aging strategies — is its tumor-suppressive activity. The Klotho gene is epigenetically silenced (promoter hypermethylation) in multiple cancer types, including breast cancer, hepatocellular carcinoma, lung cancer, and colorectal cancer. Restoring Klotho expression in these cancers suppresses proliferation, induces apoptosis, and inhibits invasion/metastasis (Zhou & Wang, 2015, Cancer Letters).

The anti-cancer mechanisms overlap with the anti-aging mechanisms:

• IGF-1/insulin signaling inhibition: Klotho suppresses the PI3K/AKT/mTOR pathway, which drives proliferation in many cancers
• Wnt signaling inhibition: Klotho sequesters Wnt ligands, suppressing Wnt/?-catenin signaling, which is activated in many epithelial cancers
• FGF signaling modulation: Klotho can inhibit FGF signaling in certain contexts, reducing mitogenic stimulation

This anti-cancer activity is a significant advantage from a safety perspective. Unlike HGF/c-Met potentiators (such as Dihexa) or direct growth factor administration, Klotho-based approaches are expected to reduce rather than increase cancer risk — a rare feature for an anti-aging intervention.

Therapeutic Strategies: Getting Klotho Into Patients

The central challenge of Klotho therapeutics is delivery. The protein is large (130 kDa for full-length, ~65 kDa for KL1 domain), expensive to produce, and cannot be taken orally. Several strategies are being pursued.

Recombinant Klotho Protein

Direct injection of recombinant Klotho protein (full-length or KL1 domain fragment) has proven effective in animal models. Unity Biotechnology and academic groups have produced GMP-grade recombinant Klotho for potential clinical use. The KL1 domain alone retains most anti-aging and cognitive-enhancing activity and is simpler to produce. Challenges include production cost, storage stability, and the need for parenteral administration (injection or infusion).

Gene Therapy

AAV (adeno-associated virus) vector-mediated delivery of the Klotho gene provides sustained Klotho overexpression from a single treatment. In mice, AAV-Klotho gene therapy produced sustained increases in circulating Klotho for months after a single injection and showed therapeutic effects in models of CKD, cardiac dysfunction, and cognitive impairment. Multiple AAV gene therapy clinical trials for other proteins have reached advanced stages, providing a regulatory and manufacturing precedent for this approach.

Small Molecules That Increase Endogenous Klotho

Several compounds have been shown to increase endogenous Klotho expression:

• HDAC inhibitors: Histone deacetylase inhibitors (vorinostat, trichostatin A) reverse the epigenetic silencing of the Klotho promoter. In CKD mice, HDAC inhibitors increased Klotho expression 2-3 fold.
• PPAR-? agonists (pioglitazone, rosiglitazone): Increase Klotho gene transcription through PPAR-? responsive elements in the Klotho promoter. Pioglitazone increased circulating Klotho by 20-30% in a small human study of CKD patients.
• Vitamin D: The vitamin D receptor has a responsive element in the Klotho promoter. Adequate vitamin D status supports Klotho expression, and deficiency reduces it.
• ACE inhibitors and ARBs: Renin-angiotensin system inhibitors increase renal Klotho expression, potentially contributing to their cardiovascular and renal protective effects beyond blood pressure reduction.

Klotho-Derived Peptides

An emerging approach is the development of shorter Klotho-derived peptide fragments that retain biological activity but are more practical to manufacture and deliver. The minimal active domain for cognitive effects appears to reside within the KL1 domain, and even shorter fragments within KL1 are being evaluated for their ability to enhance GluN2B-containing NMDA receptor function. If a peptide fragment of 20-50 amino acids retains Klotho’s cognitive-enhancing activity, it could be produced affordably and potentially delivered intranasally — a route that bypasses the BBB through olfactory and trigeminal nerve pathways.

Peptide Connections: Klotho, mTOR, NAD+, and Research Compounds

Klotho intersects with multiple pathways relevant to peptide aging research.

Klotho and mTOR

Klotho is a natural mTOR inhibitor — it suppresses insulin/IGF-1 ? PI3K ? AKT ? mTORC1 signaling. The anti-aging effects of Klotho overexpression in mice overlap significantly with those of rapamycin treatment: both extend lifespan, reduce cancer, improve immune function in aged animals, and activate autophagy. Klotho can be viewed as an endogenous upstream regulator of the same pathway that rapamycin targets pharmacologically.

Klotho and NAD+/NNMT

Klotho deficiency leads to increased oxidative stress and mitochondrial dysfunction — both of which deplete NAD+ through PARP activation and impair sirtuin function. Restoring Klotho may indirectly support NAD+ homeostasis by reducing the oxidative burden that consumes NAD+. Conversely, NNMT inhibition with 5-amino-1MQ (which boosts NAD+ and preserves SAM) may support Klotho expression by improving the epigenetic maintenance of the Klotho gene promoter — since Klotho promoter methylation is one of the age-related epigenetic changes that SAM depletion could exacerbate.

Klotho and Senescence

Klotho suppresses cellular senescence through Wnt pathway inhibition, oxidative stress reduction, and mTOR/growth signaling modulation. Klotho-deficient mice accumulate senescent cells at accelerated rates, while Klotho overexpression reduces the senescent cell burden in aged tissues. This places Klotho-based interventions in the same mechanistic space as senolytic and senomorphic strategies — complementary approaches that could be combined.

Natural Ways to Boost Klotho Levels

Exercise

Aerobic exercise is the most potent natural Klotho enhancer identified. A 2019 meta-analysis of 11 studies found that regular aerobic exercise increased circulating Klotho by 10-20% in both young and older adults. High-intensity interval training (HIIT) appeared more effective than moderate-intensity continuous training, though both showed benefit. A single bout of intense exercise can transiently increase Klotho by 15-30% for 24-48 hours post-exercise.

Vitamin D

Vitamin D receptor activation directly stimulates Klotho gene transcription. Supplementation to achieve serum 25(OH)D levels of 40-60 ng/mL has been associated with higher Klotho levels in observational studies. The relationship appears threshold-dependent — correcting deficiency produces the largest Klotho increases, while supplementation above sufficient levels shows diminishing returns.

Caloric Restriction and Fasting

Caloric restriction increases Klotho expression in animal models, likely through SIRT1-mediated deacetylation of the Klotho promoter and reduced inflammatory signaling. Intermittent fasting protocols have shown similar effects in limited human studies.

Mediterranean Diet

The Mediterranean dietary pattern (high in polyphenols, omega-3 fatty acids, and fiber; low in processed foods and refined sugars) is associated with higher circulating Klotho levels in observational studies. Specific components — including resveratrol, omega-3 fatty acids, and dietary fiber — have shown Klotho-enhancing effects in animal and cell culture models.

Stress Reduction

Chronic psychological stress is associated with lower Klotho levels. Cortisol directly suppresses Klotho gene expression through glucocorticoid receptor-mediated mechanisms. An 8-week mindfulness-based stress reduction program increased plasma Klotho by approximately 10% in a pilot study of stressed adults.

Clinical Pipeline: 2024–2026 Developments

Klotho for Cognitive Enhancement

The Dubal lab at UCSF is advancing toward a Phase I clinical trial of recombinant KL1 domain protein for age-related cognitive decline. The trial will evaluate safety, pharmacokinetics, and preliminary cognitive endpoints in healthy adults aged 65-85 with subjective cognitive complaints. If funded and approved, first dosing could occur in 2027.

Klotho for CKD

Multiple academic centers are pursuing Klotho-based strategies for chronic kidney disease — the indication with the strongest mechanistic rationale and most advanced preclinical evidence. A Phase I trial of AAV-Klotho gene therapy for advanced CKD is in planning stages at several institutions.

Klotho Biomarker Development

Standardized, clinically validated assays for circulating Klotho are being developed and commercialized. Once available in clinical laboratories, plasma Klotho measurement could become a routine biomarker of biological aging — similar to how epigenetic clocks are currently being validated. Some longevity medicine practitioners are already measuring Klotho as part of comprehensive aging panels, though assay standardization across laboratories remains an issue.

Klotho-Derived Peptide Development

At least two biotech companies have disclosed programs developing Klotho-derived peptide fragments. These shorter peptides (20-50 amino acids) are designed to retain the KL1 domain’s cognitive-enhancing activity while being more practical to manufacture and deliver (potentially intranasally). Patent filings and conference presentations suggest these programs are in late preclinical stages as of early 2026.

Frequently Asked Questions

References

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2. Kurosu H, Yamamoto M, Clark JD, et al. Suppression of aging in mice by the hormone Klotho. Science. 2005;309(5742):1829-1833. PubMed
3. Castner SA, Gupta S, Wang D, et al. Longevity factor klotho enhances cognition in aged nonhuman primates. Nature Aging. 2023;3(8):931-937. PubMed
4. Semba RD, Moghekar AR, Hu J, et al. Klotho in the cerebrospinal fluid of adults with and without Alzheimer’s disease. Neuroscience Letters. 2014;558:37-40. PubMed
5. Kuro-o M. The Klotho proteins in health and disease. Nature Reviews Nephrology. 2019;15(1):27-44. PubMed
6. Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease. Journal of the American Society of Nephrology. 2011;22(1):124-136. PubMed
7. Dubal DB, Yokoyama JS, Zhu L, et al. Life extension factor klotho enhances cognition. Cell Reports. 2014;7(4):1065-1076. PubMed
8. Zhou X, Wang X. Klotho: a novel biomarker for cancer. Journal of Cancer Research and Clinical Oncology. 2015;141(6):961-969. PubMed
9. Xu Y, Sun Z. Molecular basis of Klotho: from gene to function in aging. Endocrine Reviews. 2015;36(2):174-193. PubMed
10. Donate-Correa J, Martín-Carro B, Cannata-Andía JB, et al. Klotho, oxidative stress, and mitochondrial damage. Antioxidants. 2023;12(2):443. PubMed

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