Apelin-13, a regulator of autophagy, apoptosis and inflammation in multifaceted bone protection

Gong, Ge; Wan, Wenhui; Liu, Xinhui; Yin, Jian

doi:10.1016/j.intimp.2023.109991

Cited by 15 publications

(7 citation statements)

References 92 publications

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“…Autophagy is a unique phenomenon in eukaryotic cells that involves the degradation of damaged proteins and organelles for recycling through the lysosomal pathway. It is important to note that autophagy has both positive and negative effects ( 64 , 65 ). There are three categories of autophagy: macroautophagy, chaperone-mediated autophagy, and microautophagy.…”

Section: Ros In Autophagymentioning

confidence: 99%

ROS: Executioner of regulating cell death in spinal cord injury

Yin,

Wan,

Gong

et al. 2024

Front. Immunol.

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The damage to the central nervous system and dysfunction of the body caused by spinal cord injury (SCI) are extremely severe. The pathological process of SCI is accompanied by inflammation and injury to nerve cells. Current evidence suggests that oxidative stress, resulting from an increase in the production of reactive oxygen species (ROS) and an imbalance in its clearance, plays a significant role in the secondary damage during SCI. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulatory molecule for cellular redox. This review summarizes recent advancements in the regulation of ROS-Nrf2 signaling and focuses on the interaction between ROS and the regulation of different modes of neuronal cell death after SCI, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we highlight the pathways through which materials science, including exosomes, hydrogels, and nanomaterials, can alleviate SCI by modulating ROS production and clearance. This review provides valuable insights and directions for reducing neuronal cell death and alleviating SCI through the regulation of ROS and oxidative stress.

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Section: Ros In Autophagymentioning

confidence: 99%

ROS: Executioner of regulating cell death in spinal cord injury

Yin,

Wan,

Gong

et al. 2024

Front. Immunol.

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“…Apelin, originally identified as an adipokine, exerts its influence through the apelin/APJ axis, participating in a multifaceted spectrum of processes involving vascular integrity, cardiac functionality, renal health, and perturbations in glucose metabolism (de Oliveira et al, 2022;Li et al, 2022). Apelin modulates cell survival and differentiation in bone marrowderived mesenchymal stem cells (BMSCs) and other cell types by regulating processes such as autophagy, apoptosis, and inflammation, thereby exerting a protective role in bone-related disorders including osteoporosis, fracture healing, arthritis, and periprosthetic osteolysis (Gong et al, 2023). In addition, the expression of apelin in the uterus and ovary suggests its involvement in placental physiology and regulation of pregnancy (Dawid et al, 2021).…”

Section: Apelin and Its Peripheral Effectsmentioning

confidence: 99%

The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases

Bian,

Wang,

Wang

et al. 2024

Front. Mol. Neurosci.

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The initiation and progression of neurodegenerative diseases (NDs), distinguished by compromised nervous system integrity, profoundly disrupt the quality of life of patients, concurrently exerting a considerable strain on both the economy and the social healthcare infrastructure. Exercise has demonstrated its potential as both an effective preventive intervention and a rehabilitation approach among the emerging therapeutics targeting NDs. As the largest secretory organ, skeletal muscle possesses the capacity to secrete myokines, and these myokines can partially improve the prognosis of NDs by mediating the muscle-brain axis. Besides the well-studied exerkines, which are secreted by skeletal muscle during exercise that pivotally exert their beneficial function, the physiological function of novel exerkines, e.g., apelin, kynurenic acid (KYNA), and lactate have been underappreciated previously. Herein, this review discusses the roles of these novel exerkines and their mechanisms in regulating the progression and improvement of NDs, especially the significance of their functions in improving NDs’ prognoses through exercise. Furthermore, several myokines with potential implications in ameliorating ND progression are proposed as the future direction for investigation. Elucidation of the function of exerkines secreted by skeletal muscle in the regulation of NDs advances the understanding of its pathogenesis and facilitates the development of therapeutics that intervene in these processes to cure NDs.

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“…Toll-like receptors (TLRs) not only recognize exogenous pathogen-associated molecular patterns (PAMPs), but also detect endogenous products associated with inflammation, such as heat shock proteins, high mobility base box (HMGB) 1, fibronectin Protein and Hyaluronic Acid. Adenosine triphosphate (ATP) and ROS can further activate NLRP3, a member of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLRs) family, which intensifies and perpetuates the process of inflammation ( 93 – 95 ).…”

Section: Inhibiting Inflammationmentioning

confidence: 99%

Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis

Yin,

Gong,

Liu

et al. 2023

Front. Immunol.

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Joint replacement surgery is the most effective treatment for end-stage arthritis. Aseptic loosening caused by periprosthetic osteolysis is a common complication after joint replacement. Inflammation induced by wear particles derived from prosthetic biomaterials is a major cause of osteolysis. We emphasize that bone marrow-derived macrophages and their fusion-derived osteoclasts play a key role in this pathological process. Researchers have developed multiple intervention approaches to regulate macrophage/osteoclast activation. Aiming at wear particle-induced periprosthetic aseptic osteolysis, this review separately discusses the molecular mechanism of regulation of ROS formation and inflammatory response through intervention of macrophage/osteoclast RANKL-MAPKs-NF-κB pathway. These molecular mechanisms regulate osteoclast activation in different ways, but they are not isolated from each other. There is also a lot of crosstalk among the different mechanisms. In addition, other bone and joint diseases related to osteoclast activation are also briefly introduced. Therefore, we discuss these new findings in the context of existing work with a view to developing new strategies for wear particle-associated osteolysis based on the regulation of macrophages/osteoclasts.

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Apelin-13, a regulator of autophagy, apoptosis and inflammation in multifaceted bone protection

Cited by 15 publications

References 92 publications

ROS: Executioner of regulating cell death in spinal cord injury

ROS: Executioner of regulating cell death in spinal cord injury

The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases

Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis

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