Astaxanthin suppresses oxidative stress and calcification in vertebral cartilage endplate via activating Nrf-2/HO-1 signaling pathway

Yang, Guihe; Liu, Xiaoyang; Jing, Xingzhi; Wang, Jinjin; Wang, Heran; Chen, Feifei; Wang, Qianqian; Shao, Yuandong; Cui, Xingang

doi:10.1016/j.intimp.2023.110159

Cited by 7 publications

(6 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another study demonstrated that ASTX improves the activation of the Nrf-2/HO-1 signaling pathway, which promotes the process of mitophagy, inhibits oxidative stress and ferroptosis of cartilage endplate chondrocytes, and, finally, improves the degradation of the extracellular matrix, the calcification of cartilage endplate and endplate chondrocytes by activating apoptosis. Furthermore, ASTX inhibits the NF-κB activity induced by oxidative stimulation and can improve the inflammatory response [ 173 ]. ASTX could also protect the endplate of vertebral cartilage against oxidative stress and degeneration by activating the Nrf-2/HO-1 pathway [ 173 ].…”

Section: Molecules With Demonstrated Clinical Efficacy In the Prevent...mentioning

confidence: 99%

“…Furthermore, ASTX inhibits the NF-κB activity induced by oxidative stimulation and can improve the inflammatory response [ 173 ]. ASTX could also protect the endplate of vertebral cartilage against oxidative stress and degeneration by activating the Nrf-2/HO-1 pathway [ 173 ]. However, dysfunction of this molecular pathway is related to the development of many pathologies, such as obesity.…”

Section: Molecules With Demonstrated Clinical Efficacy In the Prevent...mentioning

confidence: 99%

See 1 more Smart Citation

Clinically Effective Molecules of Natural Origin for Obesity Prevention or Treatment

Hidalgo-Lozada,

Villarruel-López,

Nuño

et al. 2024

IJMS

View full text Add to dashboard Cite

The prevalence and incidence of obesity and the comorbidities linked to it are increasing worldwide. Current therapies for obesity and associated pathologies have proven to cause a broad number of adverse effects, and often, they are overpriced or not affordable for all patients. Among the alternatives currently available, natural bioactive compounds stand out. These are frequently contained in pharmaceutical presentations, nutraceutical products, supplements, or functional foods. The clinical evidence for these molecules is increasingly solid, among which epigallocatechin-3-gallate, ellagic acid, resveratrol, berberine, anthocyanins, probiotics, carotenoids, curcumin, silymarin, hydroxy citric acid, and α-lipoic acid stand out. The molecular mechanisms and signaling pathways of these molecules have been shown to interact with the endocrine, nervous, and gastroenteric systems. They can regulate the expression of multiple genes and proteins involved in starvation–satiety processes, activate the brown adipose tissue, decrease lipogenesis and inflammation, increase lipolysis, and improve insulin sensitivity. This review provides a comprehensive view of nature-based therapeutic options to address the increasing prevalence of obesity. It offers a valuable perspective for future research and subsequent clinical practice, addressing everything from the molecular, genetic, and physiological bases to the clinical study of bioactive compounds.

show abstract

Section: Molecules With Demonstrated Clinical Efficacy In the Prevent...mentioning

confidence: 99%

Section: Molecules With Demonstrated Clinical Efficacy In the Prevent...mentioning

confidence: 99%

Clinically Effective Molecules of Natural Origin for Obesity Prevention or Treatment

Hidalgo-Lozada,

Villarruel-López,

Nuño

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…Additional supplement with Ast could protect vertebral cartilage endplate degeneration against TBHP-induced cartilage endplate chondrocytes ferroptosis including restoring the downregulated expression of GPX4, ferritin heavy chain (FTH1) and solute carrier family 7 member 11 (SLC7A11) via activating Nrf-2/HO-1 pathway. 99 …”

Section: Therapeutic Strategies By Targeting Nrf2mentioning

confidence: 99%

The Pivotal Role of Nrf2 Signal Axis in Intervertebral Disc Degeneration

Pan,

Hou,

Deng

et al. 2023

JIR

View full text Add to dashboard Cite

Intervertebral disc degeneration (IDD) is considered as a dominant contributor to low back pain (LBP), causing severe pain, limited range of lumbar motion, physical dysfunction, and restriction of social activity. However, the specific pathological mechanisms underlying IDD remain elusive, and effective strategies to delay the pathogenesis of IDD are still unclear and limited. In recent years, some studies have found that nuclear factor erythroid 2-related factor 2 (Nrf2), an important antioxidant transcription factor, may play crucial roles in the pathogenesis and progression of age-related diseases including IDD. Nrf2 can maintain redox homeostasis and protecting nucleus pulposus (NP) cells against oxidative stress, inflammatory response, extracellular matrix (ECM) catabolism, cell senescence and cell death involving in the progression of IDD. In this review, we aim to systematically describe the vital roles and pathological mechanism of Nrf2 signaling axis in the pathogenesis of IDD, which may put forward potential therapeutic strategies for the prevention and treatment of IDD by targeting Nrf2.

show abstract

“…Oxidative stress has been demonstrated to be the leading cause of IDD. The protective effect of various phytochemicals extracted from plants, such as astaxanthin or icariin, against the development of IDD is attributed to the activation of Nrf2 signaling ( 9 , 10 ). However, to the best of our knowledge, only one study has assessed the roles of Nrf2 in CEP degeneration ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

Nrf2 protects against cartilage endplate degeneration through inhibiting NCOA4‑mediated ferritinophagy

Ma,

Lu,

Feng

et al. 2023

Int J Mol Med

Self Cite

View full text Add to dashboard Cite

Iron overload and ferroptosis are associated with intervertebral disc degeneration (IDD); however, the mechanism underlying the regulation of iron homeostasis remains to be elucidated. Nuclear factor erythroid 2-related factor 2 (Nrf2) has been reported to regulate cellular iron homeostasis; however, its impact on IDD pathology and the underlying mechanism of action requires further investigation. In the present study, immunohistochemistry analysis of Nrf2 expression in the cartilage endplate (CEP) was conducted and it was demonstrated that Nrf2 expression was increased in the CEP at the early stages of the development of IDD, whereas it was decreased at the late stages of the development of IDD. The results of western blot analysis indicated that the inadequate activation of Nrf2 may aggravate mitochondrial dysfunction and oxidative stress, thus promoting CEP chondrocyte degeneration and calcification. It was also revealed that Nrf2 was involved in TNF-α-induced CEP chondrocyte iron metabolism dysfunction and ferroptosis. Inhibition of Nrf2 expression using Nrf2 small interfering RNA could enhance the process of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy and increase ferrous ion content, which may promote CEP chondrocyte ferroptotic cell death and extracellular matrix degradation. Furthermore, a decrease in cellular iron concentration may inhibit CEP chondrocyte ferroptosis, and CEP degeneration and calcification. The present study highlights the role of the Nrf2/NCOA4 axis in chondrocyte ferroptosis and IDD pathogenesis, thus suggesting that activation of Nrf2 may be a promising strategy for IDD treatment.

show abstract

Astaxanthin suppresses oxidative stress and calcification in vertebral cartilage endplate via activating Nrf-2/HO-1 signaling pathway

Cited by 7 publications

References 35 publications

Clinically Effective Molecules of Natural Origin for Obesity Prevention or Treatment

Clinically Effective Molecules of Natural Origin for Obesity Prevention or Treatment

The Pivotal Role of Nrf2 Signal Axis in Intervertebral Disc Degeneration

Nrf2 protects against cartilage endplate degeneration through inhibiting NCOA4‑mediated ferritinophagy

Contact Info

Product

Resources

About