Nicotinamide Mononucleotide Does Not Prevent Cardiac Hypertrophy but Attenuates Cardiac Stress and Remodeling Markers in Mice Exposed to Intermittent Normobaric Hypoxia
4 affiliations
- 1Department of Bacteriology, Capital Institute of Pediatrics, Beijing 100020, China
- 2Capital Institute of Pediatrics, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100020, China
- 3State Key Laboratory of Pathogen and Biosecurity, Academy of Military Medical Sciences, Beijing 100071, China
- 4College of Food Science and Biology, Hebei University of Science and Technology, Shijiazhuang 050091, China
Abstract
Background: Nicotinamide mononucleotide (NMN) is a naturally occurring, biologically active nucleotide that serves as a crucial NAD+ precursor in various physiological conditions. Although intermittent hypoxia is known to substantially induce various health problems, whether NMN protects against injury induced by intermittent normobaric hypoxia remains unclear. Methods: In this study, mice were randomly assigned to groups under normoxia, intermittent normobaric hypoxia, and hypoxia with NMN intervention, and the effects of NMN were evaluated by examining organ indices, hematology, histopathology, and 16S rRNA gene amplicon sequencing. Results: Intermittent normobaric hypoxia significantly increased heart weight, cardiac index, right ventricular weight and index, spleen index, serum lactate dehydrogenase activity, and the cardiac expression of BNP and Myh7, indicating pathological cardiac hypertrophy and activation of a ventricular stress response. It also reduced the beta diversity of the gut microbiota and altered its composition. Although NMN intervention did not significantly affect most organ or hematological indices, except for a further increase in serum LDH activity, it significantly attenuated the hypoxia-induced expression of BNP and Myh7 in the right ventricle, restored the spleen weight and index, and changed the composition of the gut microbiota. These exploratory results indicate that NMN does not prevent intermittent normobaric hypoxia-induced cardiac hypertrophy at the organ level but mitigates cardiac stress markers, ameliorates splenic changes, and modulates the gut microbiota. Conclusions: These findings suggest that NMN produced selective molecular and systemic effects under hypoxic exposure rather than an overall protective phenotype and warrant further investigation.
Related
- Nicotinamide Mononucleotide Is Associated with Attenuation of OGD/R-Induced Pro-Inflammatory Programs in Microglia: Transcriptomic Evidence Converging on the NLRP3 Inflammasome and Lipid-Droplet-Related Molecular Signatures
- PEGylated nicotinamide mononucleotide targeted ferroptosis in acute kidney injury by suppressing FAR1 palmitoylation in an ACAA1-dependent manner.
- Fetal hypoxia causes oocyte oxidative stress damage via the Sirt3/Sod2 pathway and can be alleviated by nicotinamide mononucleotide
- Hepatoprotective Effect of Nicotinamide Mononucleotide on High‐Fat Diet‐Induced Non‐Alcoholic Fatty Liver Disease in Mice
- Gui Gan Shen Mai Yin attenuates cardiac hypertrophy and dysfunction in association with mitochondrial homeostasis and the PI3K/AKT1 signaling pathway
BibTeX
@article{wang2026nicotinamide,
title = {{Nicotinamide Mononucleotide Does Not Prevent Cardiac Hypertrophy but Attenuates Cardiac Stress and Remodeling Markers in Mice Exposed to Intermittent Normobaric Hypoxia}},
author = {Zhen Wang and Mingxuan Wang and Jingling Guo and Yajing Wang and Shijie Wang and Jing Yuan and Ruifu Yang and Yujing Bi and Yuehua Ke},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18203334},
url = {https://www.mdpi.com/2072-6643/18/20/3334},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Nicotinamide Mononucleotide Does Not Prevent Cardiac Hypertrophy but Attenuates Cardiac Stress and Remodeling Markers in Mice Exposed to Intermittent Normobaric Hypoxia
AU - Zhen Wang
AU - Mingxuan Wang
AU - Jingling Guo
AU - Yajing Wang
AU - Shijie Wang
AU - Jing Yuan
AU - Ruifu Yang
AU - Yujing Bi
AU - Yuehua Ke
PY - 2026
DA - 2026/10/01
JO - Nutrients
DO - 10.3390/nu18203334
UR - https://www.mdpi.com/2072-6643/18/20/3334
AB - Background: Nicotinamide mononucleotide (NMN) is a naturally occurring, biologically active nucleotide that serves as a crucial NAD+ precursor in various physiological conditions. Although intermittent hypoxia is known to substantially induce various health problems, whether NMN protects against injury induced by intermittent normobaric hypoxia remains unclear. Methods: In this study, mice were randomly assigned to groups under normoxia, intermittent normobaric hypoxia, and hypoxia with NMN intervention, and the effects of NMN were evaluated by examining organ indices, hematology, histopathology, and 16S rRNA gene amplicon sequencing. Results: Intermittent normobaric hypoxia significantly increased heart weight, cardiac index, right ventricular weight and index, spleen index, serum lactate dehydrogenase activity, and the cardiac expression of BNP and Myh7, indicating pathological cardiac hypertrophy and activation of a ventricular stress response. It also reduced the beta diversity of the gut microbiota and altered its composition. Although NMN intervention did not significantly affect most organ or hematological indices, except for a further increase in serum LDH activity, it significantly attenuated the hypoxia-induced expression of BNP and Myh7 in the right ventricle, restored the spleen weight and index, and changed the composition of the gut microbiota. These exploratory results indicate that NMN does not prevent intermittent normobaric hypoxia-induced cardiac hypertrophy at the organ level but mitigates cardiac stress markers, ameliorates splenic changes, and modulates the gut microbiota. Conclusions: These findings suggest that NMN produced selective molecular and systemic effects under hypoxic exposure rather than an overall protective phenotype and warrant further investigation.
SN - 2072-6643
ER -