The NOS/NO System in Renal Programming and Reprogramming

You-Lin Tain1,2,3, Chien-Ning Hsu4,5

  • 1Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.

PubMed

Insights

Nitric oxide (NO) deficiency is linked to chronic kidney disease (CKD) risk via renal programming. Early interventions targeting NO show promise for preventing CKD in preclinical models.

Area of Science:

  • Nephrology
  • Developmental Biology
  • Biochemistry

Background:

  • Nitric oxide (NO), a key signaling molecule, possesses renoprotective effects.
  • NO deficiency is implicated in chronic kidney disease (CKD) pathogenesis.
  • Adverse intrauterine conditions can lead to renal programming, increasing adult CKD risk.

Purpose of the Study:

  • To review nitric oxide synthase (NOS)/NO research in renal programming and reprogramming.
  • To explore the interaction between NO deficiency and mechanisms of renal programming.
  • To assess the potential of NO-targeting strategies for reprogramming.

Main Methods:

  • Literature review of NOS/NO research in renal programming.
  • Analysis of preclinical studies on NO supplementation and related interventions.
  • Examination of molecular mechanisms linking NO to renal programming.

Main Results:

  • NO deficiency interacts with oxidative stress, renin-angiotensin system dysfunction, nutrient sensing, hydrogen sulfide signaling, and gut dysbiosis in renal programming.
  • Interventions like NOS substrate supplementation, ADMA inhibition, NO donor administration, and enhanced NOS during gestation/lactation show benefits in preclinical models.
  • Experimental data suggest NO targeting as a viable reprogramming strategy.

Conclusions:

  • NO plays a critical role in mitigating renal programming-induced kidney disease.
  • Targeting NO pathways offers a promising therapeutic avenue for reprogramming detrimental developmental insults.
  • Further research, including human studies, is needed to validate NO-based interventions for preventing CKD.

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