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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.

Antioxidants (Basel, Switzerland)
|August 26, 2023
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
asymmetric dimethylargininedevelopmental origins of health and disease (DOHaD)hypertensionkidney diseasenitric oxidenitric oxide synthaseoxidative stressrenal programming

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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.