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Mitochondria and NLRP3 inflammasome in cardiac hypertrophy

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Abstract

Cardiac hypertrophy is the main adaptive response of the heart to chronic loads; however, prolonged or excessive hypertrophy promotes myocardial interstitial fibrosis, systolic dysfunction, and cardiomyocyte death, especially aseptic inflammation mediated by NLRP3 inflammasome, which can aggravate ventricular remodeling and myocardial damage, which is an important mechanism for the progression of heart failure. Various cardiac overloads can cause mitochondrial damage. In recent years, the mitochondria have been demonstrated to be involved in the inflammatory response during the development of cardiac hypertrophy in vitro and in vivo. As the NLRP3 inflammasome and mitochondria are regulators of inflammation and cardiac hypertrophy, we explored the potential functions of the NLRP3 inflammasome and mitochondrial dysfunction in cardiac hypertrophy. In particular, we proposed that the induction of mitochondrial dysfunction in cardiomyocytes may promote NLRP3-dependent inflammation during myocardial hypertrophy. Further in-depth studies could prompt valuable discoveries regarding the underlying molecular mechanisms of cardiac hypertrophy, reveal novel anti-inflammatory therapies for cardiac hypertrophy, and provide more desirable therapeutic outcomes for patients with cardiac hypertrophy.

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Abbreviations

ACEI:

Angiotensin-converting enzyme

ASC:

Apoptosis-associated speck-like protein containing a CARD

ATP:

Adenosine triphosphate

DAMPs:

Danger-associated molecular patterns

GSDMD:

Gasdermin D

GSDMD-NT:

GSDMD-N-terminal

IF1:

Inhibitory factor 1

IL-1β:

Interleukin-1β

IL-1R1:

IL-1 receptor type 1

IL-18:

Interleukin-18

IRI:

Ischemia-reperfusion injury

mtDNA:

Mitochondrial DNA

mt-dynamics:

Mitochondrial dynamics

NF-κB:

Nuclear factor-κB

NLRP3:

The pyridine domain-containing 3

NLRs:

Nucleotide-binding and oligomerization domain (NOD)-like receptor

NOX:

Nicotinamide adenine dinucleotide phosphate oxidase

Ox-mtDNA:

Oxidation of mtDNA

PPQ:

Pyrroloquinoline quinone

ROS:

Reactive oxygen species

SiNP:

Silica nanoparticle

SUMO:

Small ubiquitin-related modifier

TNF:

Tumor necrosis factor

TNFR:

Tumor necrosis factor receptor

TLR4:

Toll-like receptor 4

YLLs:

Years of life lost

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Funding

This work was supported by Jilin Provincial Science and Technology Commission International Science and Technology Cooperation (Grant No. 20230402015GH), Jilin Provincial Department of Finance (Grant No. 2021SCZ24), and Jilin Provincial Science and Technology Development Plan Project (Grant No. 20210101258JC).

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Authors and Affiliations

  1. Department of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, NO.990 Qinghua Street, Changchun, Jilin, China

    Ruyu Yan, Yifan Yang, Yujiao Jiang & Yan Meng

  2. Department of Pathology, Zhuzhou Central Hospital, Zhuzhou, Hunan, China

    Ruyu Yan

  3. Department of Otorhinolaryngology-Head and Neck Surgery, China-Japan Union Hospital, Jilin University, Changchun, China

    Yuxin Sun

  4. Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China

    Rongchao Zhang

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  1. Ruyu Yan
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  2. Yuxin Sun
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  3. Yifan Yang
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  4. Rongchao Zhang
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  5. Yujiao Jiang
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  6. Yan Meng
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Contributions

YM proposed conceptualization. RY drafted the manuscript. YS and YY assisted RY in screening articles. YJ and RZ created computer graphics and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

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Correspondence to Yan Meng.

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Yan, R., Sun, Y., Yang, Y. et al. Mitochondria and NLRP3 inflammasome in cardiac hypertrophy. Mol Cell Biochem (2023). https://doi.org/10.1007/s11010-023-04812-1

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