Improving Lysosomal Ferroptosis via NMN Administration to Prevent Heart Failure

Deciphering Another Mechanism of Action for NMN Administration: Improving Lysosomal Ferroptosis to Prevent Heart Failure



1. Introduction

     Heart failure is a serious condition in the development of cardiovascular disease. In particular, diastolic heart failure, as one of the most common manifestations of heart failure in the elderly, has always been viewed as a classic aging-related terminal illness due to its high prevalence and lack of effective treatment. 
    N
icotinamide mononucleotide (NMN)  raises the hope for the treatment of this illness.  NMN can restore the functions of heart and blood vessels, protect the heart from damage after a heart attack, prevent heart failure by promoting the health of the mitochondria, and restore cardiovascular, cognitive, and metabolic decline.
    This study is dedicated to deciphering another mechanism of action for NMN administration, namely improving lysosomal ferroptosis to prevent heart failure. 

2. The key pathogenesis of diastolic heart failure

    The effect of NMN on improving cardiac function is mainly realized by elevating the level of myocardial nicotinamide adenine dinucleotide (NAD+), an important coenzyme in the tricarboxylic acid cycle. The mitochondrial dysfunction and decreased ability of  NADbiosynthesis are the key pathogenesis of diastolic heart failure. 

3. Restoration of lysosomal function and autophagic function by NMN administration

    Lysosomal function is impaired owing to decreased NAD+ biosynthesis in vivo. NMN administration improves lysosomal function and activates amino acid metabolism in the mice with cardiomyocyte-specific knockout of p32 (p32cKO), yet barely affects the lysosomal morphology. Additionally, NMN administration improves the degradation mechanism of autophagy, as evidenced by the restoration of autophagic function post NMN administration.

4. The detailed mechanism of action for NMN administration on heart failure 

    NMN administration does not restore functional mitochondrial damage caused by the inhibition of mitochondrial translation. These findings suggest that NMN administration improves heart failure by improving lysosomal function without improving mitochondrial function.

5. The involvement of ferroptosis in heart-specific mitochondrial translation defect 

    The suppression of ferroptosis ameliorates heart failure. The expression levels of ferroptosis-related factors (Chac1, GPX4, and Ho1) are also diminished by NMN, indicating that ferroptosis in the p32cKO heart is improved by NMN administration.
 

6. The improvement of mitochondrial dysfunction-induced ferroptosis by NMN administration

   
    The ferroptosis is induced in the p32 knockdown cells, as attested by the mitochondrial translation defect and the downregulation of intracellular NAD+ and NADH levels. The induction of ferroptosis in lysosome is closely related to the amount of NAD+ biosynthesis. When intracellular NAD+ level is lowered, the intracellular iron deposition and lipid peroxide are induced, which however are ameliorated by NMN administration.

7. Conclusion

    Mechanically, NMN administration can prevent heart failure by improving lysosomal ferroptosis, opening up new insight for the treatment of this illness.

Reference

Yagi, Mikako et al. “Improving lysosomal ferroptosis with NMN administration protects against heart failure.” Life science alliance vol. 6,12 e202302116. 4 Oct. 2023, doi:10.26508/lsa.202302116

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Disclaimer

This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC.

 
 



 

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