Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging

Wan, Wei; Zhang, Lieliang; Lin, Yong; Rao, Xiuqing; Wang, Xifeng; Hua, Fuzhou; Ying, Jun

doi:10.1186/s12967-023-03885-2

Cited by 15 publications

(13 citation statements)

References 109 publications

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“…Through these, mitochondria regulate not only energy production but a cellular homeostasis that includes a range of processes such as immune/inflammatory responses, proteostasis, adaptive responses to stress, and apoptosis [ 96 , 97 , 98 ]. Muscle humanin expression is upregulated in humans, in response to exercise stress, mtDNA mutation-associated diseases, and healthy aging, suggesting a tissue-specific response aimed at restoring mitochondrial homeostasis [ 102 ] in response to stress from, for example, acute exercise [ 102 ]. Several skeletal muscle diseases are manifested by either an excess of leading to atrophy, or a reduced autophagy mechanism leading to muscle and mitochondrial degeneration [ 103 ].…”

Section: Resultsmentioning

confidence: 99%

Humanin and Its Pathophysiological Roles in Aging: A Systematic Review

Coradduzza

Congiargiu

Chen

et al. 2023

Biology

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Background: Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased cellular damage and death. These conditions play an essential role in aging and significantly contribute to the development of age-related complications. Humanin is a mitochondrial-derived peptide (MDP), encoded by mitochondrial DNA, playing a cytoprotective role to preserve mitochondrial function and cell viability under stressful and senescence conditions. For these reasons, humanin can be exploited in strategies aiming to counteract several processes involved in aging, including cardiovascular disease, neurodegeneration, and cancer. Relevance of these conditions to aging and disease: Senescence appears to be involved in the decay in organ and tissue function, it has also been related to the development of age-related diseases, such as cardiovascular conditions, cancer, and diabetes. In particular, senescent cells produce inflammatory cytokines and other pro-inflammatory molecules that can participate to the development of such diseases. Humanin, on the other hand, seems to contrast the development of such conditions, and it is also known to play a role in these diseases by promoting the death of damaged or malfunctioning cells and contributing to the inflammation often associated with them. Both senescence and humanin-related mechanisms are complex processes that have not been fully clarified yet. Further research is needed to thoroughly understand the role of such processes in aging and disease and identify potential interventions to target them in order to prevent or treat age-related conditions. Objectives: This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, humanin, aging, and disease.

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Section: Resultsmentioning

confidence: 99%

Humanin and Its Pathophysiological Roles in Aging: A Systematic Review

Coradduzza

Congiargiu

Chen

et al. 2023

Biology

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“…Proliferator-Activated Receptor Gamma Coactivator 1-Alpha (PGC1α) pathways. 117 MDPs have demonstrated diverse functions as cytoprotective agents, such as regulating apoptosis, inflammation, and ROS in vitro and in vivo. 118 These functions strongly connect MDPs and CVD risk factors (atherosclerosis, hyperlipidaemia, insulin resistance, and aging).…”

Section: Mitochondria Targeting Moieties and Therapeutic Peptidesmentioning

confidence: 99%

“…NH stimulates the expression of superoxide dismutase 1 (SOD1) 115 and restores glutathione (known as cardioprotectors 116 ). MOTS‐c is reported to act throughout AMP‐activated protein kinase (AMPK), Sirtuin 1 (SIRT1), and Peroxisome Proliferator‐Activated Receptor Gamma Coactivator 1‐Alpha (PGC1α) pathways 117 . MDPs have demonstrated diverse functions as cytoprotective agents, such as regulating apoptosis, inflammation, and ROS in vitro and in vivo 118 .…”

Section: Nanoparticle‐based Strategies For Targeting Mitochondria To ...mentioning

confidence: 99%

Nanoparticle‐based therapeutic strategies for mitochondrial dysfunction in cardiovascular disease

Suzuki,

Xing,

Giblin

et al. 2024

J Biomedical Materials Res

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Although cardiovascular diseases (CVD) are the leading cause of global mortality, there is a lack of therapies that target and revert underlying pathological processes. Mitochondrial dysfunction is involved in the pathophysiology of CVD, and thus is a potential target for therapeutic development. To target the mitochondria and improve therapeutic efficacy, nanoparticle‐based delivery systems have been proposed as promising strategies for the delivery of therapeutic agents to the mitochondria. This review will first discuss how mitochondrial dysfunction is related to the progression of several CVD and then delineate recent progress in mitochondrial targeting using nanoparticle‐based delivery systems including peptide‐based nanosystems, polymeric nanoparticles, liposomes, and lipid nanoparticles. In addition, we summarize the advantages of these nanocarriers and remaining challenges in targeting the mitochondria as a therapeutic strategy for CVD treatment.

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“…Consequently, they directly impact ATP production and cellular energy homeostasis. Disruptions in these modifications can lead to mitochondrial dysfunction, contributing to various metabolic and neurodegenerative diseases 84 . Thus, mitochondrial rRNA modifications are crucial for maintaining cellular energy balance and mitochondrial health.…”

Section: Mitochondrial Rrna Modificationmentioning

confidence: 99%

Decoding the ribosome's hidden language: rRNA modifications as key players in cancer dynamics and targeted therapies

Cui,

Zheng,

Lin

et al. 2024

Clinical & Translational Med

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Ribosomal RNA (rRNA) modifications, essential components of ribosome structure and function, significantly impact cellular proteomics and cancer biology. These chemical modifications transcend structural roles, critically shaping ribosome functionality and influencing cellular protein profiles. In this review, the mechanisms by which rRNA modifications regulate both rRNA functions and broader cellular physiological processes are critically discussed. Importantly, by altering the translational output, rRNA modifications can shift the cellular equilibrium towards oncogenesis, thus playing a key role in cancer development and progression. Moreover, a special focus is placed on the functions of mitochondrial rRNA modifications and their aberrant expression in cancer, an area with profound implications yet largely uncharted. Dysregulation in these modifications can lead to metabolic dysfunction and apoptosis resistance, hallmark traits of cancer cells. Furthermore, the current challenges and future perspectives in targeting rRNA modifications are highlighted as a therapeutic approach for cancer treatment. In conclusion, rRNA modifications represent a frontier in cancer research, offering novel insights and therapeutic possibilities. Understanding and harnessing these modifications can pave the way for breakthroughs in cancer treatment, potentially transforming the approach to combating this complex disease.

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Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging

Cited by 15 publications

References 109 publications

Humanin and Its Pathophysiological Roles in Aging: A Systematic Review

Humanin and Its Pathophysiological Roles in Aging: A Systematic Review

Nanoparticle‐based therapeutic strategies for mitochondrial dysfunction in cardiovascular disease

Decoding the ribosome's hidden language: rRNA modifications as key players in cancer dynamics and targeted therapies

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