ArticleJCI insight2019
FGF23 expression is stimulated in transgenic α-Klotho longevity mouse model.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Antiaging Properties of the Klotho Protein.Cells · 2026Review
- Integrin CD11b Alleviates Cerebral Ischemia/Reperfusion Injury via a Mechanism Involving Microglia/Macrophage Polarization.Journal of molecular neuroscience : MN · 2025Article
- Klotho plasma levels are an independent predictorof mortality in women with acute coronary syndrome.Scientific reports · 2025Article
- Klotho antiaging protein: molecular mechanisms and therapeutic potential in diseases.Molecular biomedicine · 2025Review
- Association between pan-immune-inflammation value and Serum Klotho levels: a cross-sectional analysis of renal function mediation.Frontiers in immunology · 2025Article
- Klotho: A Large Protein with Various Beneficial Functions, but also with Therapeutic Value?Journal of the American Society of Nephrology : JASN · 2024Article
- FGF23 and klotho at the intersection of kidney and cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Distinct role of Klotho in long bone and craniofacial bone: skeletal development, repair and regeneration.PeerJ · 2024Review
- Molecular Interaction of Soluble Klotho with FGF23 in the Pathobiology of Aortic Valve Lesions Induced by Chronic Kidney Disease.International journal of biological sciences · 2024Article
- Structural asymmetry in FGF23 signaling.Trends in pharmacological sciences · 2023Article
- Platelet factors are induced by longevity factor klotho and enhance cognition in young and aging mice.Nature aging · 2023Article
- FGF23 alleviates neuronal apoptosis and inflammation, and promotes locomotion recovery via activation of PI3K/AKT signalling in spinal cord injury.Experimental and therapeutic medicine · 2023Article
- Differential toxicity profile of secreted and processed α-Klotho expression over mineral metabolism and bone microstructure.Scientific reports · 2023Article
- The fibroblast growth factor-Klotho axis at molecular level.Open life sciences · 2023Review
- Current and Future Therapeutical Aspects of X-Linked Hypophosphatemia in Children With Special Attention to Klotho/Fibroblast Growth Factor 23 System.Journal of clinical medicine research · 2022Article
- Soluble α-klotho and heparin modulate the pathologic cardiac actions of fibroblast growth factor 23 in chronic kidney disease.Kidney international · 2022Article
- The role of microglial/macrophagic salt-inducible kinase 3 on normal and excessive phagocytosis after transient focal cerebral ischemia.Cellular and molecular life sciences : CMLS · 2022Article
- Klotho Modulates Pro-Fibrotic Activities in Human Atrial Fibroblasts through Inhibition of Phospholipase C Signaling and Suppression of Store-Operated Calcium Entry.Biomedicines · 2022Article
- Article
- Pathophysiology and genetics of salt-sensitive hypertension.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Observations in transgenic α-Klotho (Kl) mice (KlTg) defined the antiaging role of soluble Klotho (sKL130). A genetic translocation that elevates sKL levels in humans is paradoxically associated with increased circulating fibroblast growth factor 23 (FGF23) levels and the potential of both membrane KL (mKL135) and sKL130 to act as coreceptors for FGF23 activation of fibroblast growth factor receptors (FGFRs). Neither FGF23 expression nor the contributions of FGF23, mKL135, and sKL130 codependent and independent functions have been investigated in KlTg mice. In the current study, we examined the effects of Kl overexpression on FGF23 levels and functions in KlTg mice. We found that mKL135 but not sKL130 stimulated FGF23 expression in osteoblasts, leading to elevated Fgf23 bone expression and circulating levels in KlTg mice. Elevated FGF23 suppressed 1,25(OH)2D and parathyroid hormone levels but did not cause hypophosphatemic rickets in KlTg mice. KlTg mice developed low aldosterone-associated hypertension but not left ventricular hypertrophy. Mechanistically, we found that mKL135 and sKL130 are essential cofactors for FGF23-mediated ERK activation but that they inhibited FGF23 stimulation of PLC-γ and PI3K/AKT signaling. Thus, increased longevity in KlTg mice occurs in the presence of excess FGF23 that interacts with mKL and sKL to bias FGFR pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.