ragu
illuminati
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- Jul 9, 2025
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so ive already made thread about this but it didnt get recognition it deserved
WHAT IS KLOTHO
there is two type of klotho protein
1.co-receptor
2.soluble hormone-like protein
WHAT DOES CO-RECEPTOR KLOTHO DO
Klotho sits on the surface of kidney cells and partners with the FGF receptor (FGFR1c). On its own, FGFR1c binds FGF23 poorly. Klotho essentially acts like an adapter that lets FGF23 dock properly onto its receptor, which is what triggers the phosphate-excretion signal in the kidney.
WHAT DOES HORMONE-PROTEIN LIKE KLOTHO DO
Klotho can also be cleaved off the cell membrane and released into the bloodstream. In this free-floating form, it acts more broadly around the body — independent of FGF23 — and has been studied for effects like:
1.Anti-aging properties
2.Antioxidant and anti-inflammatory effects
3.Anti-fibrotic effects in the kidney and heart
4.Regulating calcium channels
WHY DOES IT MATTER
Klotho levels tend to decline early in chronic kidney disease often before other markers change and low Klotho is associated with faster kidney disease progression, vascular calcification, and cardiac problems. That's why it's being explored as a biomarker and, as we discussed, as a potential future therapy (recombinant Klotho), though nothing is approved for clinical use yet.
CAN IT PREVENT BLINDESS CAUSED BY ERDA
no retards there isnt any studies about how it can prevent blindness as i said in the co receptor klotho FGF23 (secreted by osteocytes/osteoblasts) binds the KLOTHO-FGFR1c co-receptor complex in the kidney. This activates the FRS2/RAS/RAF/MEK/ERK1/2 signaling cascade, which downregulates the phosphate transporters NPT2a and NPT2c in the proximal tubule. Result: increased urinary phosphate excretion, decreased serum phosphate. FGF23 also suppresses 1,25-dihydroxyvitamin D synthesis, reducing intestinal phosphate absorption.
Erdafitinib is a pan-FGFR (FGFR1-4) tyrosine kinase inhibitor. It doesn't block KLOTHO or FGF23 binding — it inhibits the intracellular kinase domain of FGFR, preventing downstream signal transduction after FGF23-KLOTHO-FGFR1c binding occur
With FGFR kinase activity blocked, NPT2a/NPT2c aren't downregulated, so phosphate reabsorption continues unchecked. Serum phosphate rises. This is an on-target, expected pharmacodynamic effect, not off-target toxicity.
Elevated phosphate stimulates further FGF23 secretion (via the body's normal feedback loop), so circulating FGF23 rises alongside phosphate, but remains functionally ineffective due to the kinase blockade downstream.
CONCLUSION
idk why it was blowing up on tt while not even preventing any of the sides idk what studies or hallucination they saw or experienced but if you came across any one talking about klotho and its preventing of blindness scroll away because its total bullshit
WHAT IS KLOTHO
there is two type of klotho protein
1.co-receptor
2.soluble hormone-like protein
WHAT DOES CO-RECEPTOR KLOTHO DO
Klotho sits on the surface of kidney cells and partners with the FGF receptor (FGFR1c). On its own, FGFR1c binds FGF23 poorly. Klotho essentially acts like an adapter that lets FGF23 dock properly onto its receptor, which is what triggers the phosphate-excretion signal in the kidney.
WHAT DOES HORMONE-PROTEIN LIKE KLOTHO DO
Klotho can also be cleaved off the cell membrane and released into the bloodstream. In this free-floating form, it acts more broadly around the body — independent of FGF23 — and has been studied for effects like:
1.Anti-aging properties
2.Antioxidant and anti-inflammatory effects
3.Anti-fibrotic effects in the kidney and heart
4.Regulating calcium channels
WHY DOES IT MATTER
Klotho levels tend to decline early in chronic kidney disease often before other markers change and low Klotho is associated with faster kidney disease progression, vascular calcification, and cardiac problems. That's why it's being explored as a biomarker and, as we discussed, as a potential future therapy (recombinant Klotho), though nothing is approved for clinical use yet.
CAN IT PREVENT BLINDESS CAUSED BY ERDA
no retards there isnt any studies about how it can prevent blindness as i said in the co receptor klotho FGF23 (secreted by osteocytes/osteoblasts) binds the KLOTHO-FGFR1c co-receptor complex in the kidney. This activates the FRS2/RAS/RAF/MEK/ERK1/2 signaling cascade, which downregulates the phosphate transporters NPT2a and NPT2c in the proximal tubule. Result: increased urinary phosphate excretion, decreased serum phosphate. FGF23 also suppresses 1,25-dihydroxyvitamin D synthesis, reducing intestinal phosphate absorption.
Erdafitinib is a pan-FGFR (FGFR1-4) tyrosine kinase inhibitor. It doesn't block KLOTHO or FGF23 binding — it inhibits the intracellular kinase domain of FGFR, preventing downstream signal transduction after FGF23-KLOTHO-FGFR1c binding occur
With FGFR kinase activity blocked, NPT2a/NPT2c aren't downregulated, so phosphate reabsorption continues unchecked. Serum phosphate rises. This is an on-target, expected pharmacodynamic effect, not off-target toxicity.
Elevated phosphate stimulates further FGF23 secretion (via the body's normal feedback loop), so circulating FGF23 rises alongside phosphate, but remains functionally ineffective due to the kinase blockade downstream.
CONCLUSION
idk why it was blowing up on tt while not even preventing any of the sides
idk what studies or hallucination they saw or experienced but if you came across any one talking about klotho and its preventing of blindness scroll away because its total bullshit
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