ReviewCellular and molecular life sciences : CMLS2019
αKlotho-FGF23 interactions and their role in kidney disease: a molecular insight.
Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Association between soluble Klotho levels and calcification propensity T50 in patients with hemodialysis: a cross-sectional study.Scientific reports · 2026Article
- Antiaging Properties of the Klotho Protein.Cells · 2026Review
- Study of Molecular Docking and Evolutionary Dynamics of the FGF Gene Family in Nile Tilapia.Marine biotechnology (New York, N.Y.) · 2025Article
- Review
- Women With a History of Preeclampsia Exhibit Accelerated Aging and Unfavorable Profiles of Senescence Markers.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- New concepts in regulation and function of the FGF23.Clinical and experimental medicine · 2023Review
- Neuroprotective Role of Klotho on Dementia.Cureus · 2023Review
- Hypoxia-Induced Kidney Injury in Newborn Rats.Toxics · 2023Article
- Zebrafish Models to Study Ectopic Calcification and Calcium-Associated Pathologies.International journal of molecular sciences · 2023Review
- The fibroblast growth factor-Klotho axis at molecular level.Open life sciences · 2023Review
- Vascular Calcification in Chronic Kidney Disease: An Update and Perspective.Aging and disease · 2022Article
- Changes of FGF23 and the Renin-Angiotensin-System in Male Mouse Models of Chronic Kidney Disease and Cardiac Hypertrophy.Journal of the Endocrine Society · 2022Article
- Role of KInternational journal of molecular sciences · 2021Review
- Reduction of Calciprotein Particles in Adults Receiving Infliximab for Chronic Inflammatory Disease.JBMR plus · 2021Article
- The Importance of Phosphate Control in Chronic Kidney Disease.Nutrients · 2021Review
- Design and methodology of the Aging Nephropathy Study (AGNES): a prospective cohort study of elderly patients with chronic kidney disease.BMC nephrology · 2020Article
- Peroxisome proliferator-activated receptor α (PPARα)-dependent regulation of fibroblast growth factor 23 (FGF23).Pflugers Archiv : European journal of physiology · 2020Article
- Review
- Klotho, Aging, and the Failing Kidney.Frontiers in endocrinology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Following the serendipitous discovery of the ageing suppressor, αKlotho (αKl), several decades ago, a growing body of evidence has defined a pivotal role for its various forms in multiple aspects of vertebrate physiology and pathology. The transmembrane form of αKl serves as a co-receptor for the osteocyte-derived mineral regulator, fibroblast growth factor (FGF)23, principally in the renal tubules. However, compelling data also suggest that circulating soluble forms of αKl, derived from the same source, may have independent homeostatic functions either as a hormone, glycan-cleaving enzyme or lectin. Chronic kidney disease (CKD) is of particular interest as disruption of the FGF23-αKl axis is an early and common feature of disease manifesting in markedly deficient αKl expression, but FGF23 excess. Here we critically discuss recent findings in αKl biology that conflict with the view that soluble αKl has substantive functions independent of FGF23 signalling. Although the issue of whether soluble αKl can act without FGF23 has yet to be resolved, we explore the potential significance of these contrary findings in the context of CKD and highlight how this endocrine pathway represents a promising target for novel anti-ageing therapeutics.
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What OpenQuestion holds
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.