From the Guidelines
Klotho medicine is not currently approved for medical use, and its therapeutic applications are still under experimental investigation. The Klotho protein has been identified as a key regulator of mineral metabolism, and its decline with age has been linked to various diseases, including chronic kidney disease [ 1 ]. Research has shown that Klotho plays a crucial role in regulating phosphate levels, and its interaction with FGF23 is essential for maintaining normal phosphate homeostasis [ 1 ]. However, the use of Klotho as a therapeutic target is still in its infancy, and more research is needed to fully understand its potential benefits and risks.
Some studies have investigated the use of phosphate-lowering therapies in patients with chronic kidney disease (CKD), including those with normal phosphate levels [ 1 ]. These studies have shown that restricting the dose of calcium-based phosphate binders may be beneficial in patients with CKD [ 1 ]. However, the role of Klotho in these therapies is not yet fully understood, and more research is needed to determine its potential as a therapeutic target.
In terms of supporting Klotho levels naturally, some research suggests that regular exercise, adequate vitamin D, and possibly certain plant compounds may help maintain Klotho expression [ 1 ]. However, these approaches are not direct Klotho medicine, and their effects are modest compared to potential pharmaceutical interventions being researched. Therefore, patients should not rely solely on these natural approaches for treating or preventing diseases related to Klotho deficiency.
Key points to consider:
- Klotho medicine is not currently approved for medical use
- Klotho plays a crucial role in regulating phosphate levels and mineral metabolism
- Restricting the dose of calcium-based phosphate binders may be beneficial in patients with CKD
- Natural approaches to supporting Klotho levels, such as exercise and vitamin D, may have modest effects but are not a replacement for potential pharmaceutical interventions.
From the Research
Klotho Medicine Overview
- Klotho is recognized as an aging-suppressor protein that is implicated in various processes and signaling pathways, including anti-inflammatory, anti-apoptotic, anti-oxidant, and anti-tumor bioactivities 2.
- The protein has been found to have a role in regulating autophagy, which is the process by which eukaryotic cells clear away dysfunctional proteins and damaged organelles 3.
- Klotho deficiency has been associated with various aging-related disorders, and upregulating the Klotho gene may be a possible therapeutic and/or preventive approach in aging-related complications 4.
Therapeutic Potential of Klotho
- Klotho has been identified as a potential therapeutic target in central nervous system (CNS) diseases such as amyotrophic lateral sclerosis, Parkinson's disease, stroke, and Alzheimer's disease 2.
- The upregulation of klotho expression has been found to regulate various signaling pathways related to autophagy, oxidative stress, inflammation, cognition, and ferroptosis in neurological disorders 2.
- Klotho-enhancement strategies, including hormonal compounds, renin-angiotensin system inhibitors, antioxidants, and gene therapy, have been proposed as potential therapeutic approaches 4.
Klotho and Physical Function
- Klotho has been found to be involved in several key processes that regulate skeletal muscle function, such as muscle regeneration, mitochondrial biogenesis, endothelial function, oxidative stress, and inflammation 5.
- Emerging data support the existence of Klotho-related benefits to exercise and potential Klotho-based therapeutic interventions for the treatment of sarcopenia and its progression to physical disability 5.
Klotho and Hypertension
- Soluble klotho has been found to be protective against the development of hypertension in preclinical studies, and higher baseline serum klotho levels have been associated with a lower rate of incident hypertension 6.
- Higher klotho levels have also been associated with lower subsequent systolic and diastolic blood pressure trajectories during follow-up 6.