Celastrol: The new dawn in the treatment of vascular remodeling diseases

Tan, Jun-Lan; Jiang, Yi; Cao, Xian-Ya; Wang, Fei-Ying; Xie, Silin; Zhou, Lingling; Qin, Li; Dai, Aiguo

doi:10.1016/j.biopha.2022.114177

Cited by 6 publications

(2 citation statements)

References 129 publications

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“…Furthermore, our research discovered that CEL triggers autophagy by controlling the AMPK-mTOR-TFEB axis. CEL has a powerful antivascular remodeling effect (J. L. Tan et al, 2023). First, in antitumor research, Celastrol inhibits angiogenesis in various tumor diseases (Choi et al, 2016;Pang et al, 2010), which restrains the growth and progression of tumors in anticancer studies.…”

Section: Discussionmentioning

confidence: 99%

Celastrol enhances the viability of random‐pattern skin flaps by regulating autophagy through the AMPK‐mTOR‐TFEB axis

Gu,

Li,

Deng

et al. 2024

Phytotherapy Research

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In reconstructive and plastic surgery, random‐pattern skin flaps (RPSF) are often used to correct defects. However, their clinical usefulness is limited due to their susceptibility to necrosis, especially on the distal side of the RPSF. This study validates the protective effect of celastrol (CEL) on flap viability and explores in terms of underlying mechanisms of action. The viability of different groups of RPSF was evaluated by survival zone analysis, laser doppler blood flow, and histological analysis. The effects of CEL on flap angiogenesis, apoptosis, oxidative stress, and autophagy were evaluated by Western blot, immunohistochemistry, and immunofluorescence assays. Finally, its mechanistic aspects were explored by autophagy inhibitor and Adenosine 5′‐monophosphate (AMP)‐activated protein kinase (AMPK) inhibitor. On the seventh day after surgery, the survival area size, blood supply, and microvessel count of RPSF were augmented following the administration of CEL. Additionally, CEL stimulated angiogenesis, suppressed apoptosis, and lowered oxidative stress levels immediately after elevated autophagy in ischemic regions; These effects can be reversed using the autophagy inhibitor chloroquine (CQ). Specifically, CQ has been observed to counteract the protective impact of CEL on the RPSF. Moreover, it has also been discovered that CEL triggers the AMPK‐mTOR‐TFEB axis activation in the area affected by ischemia. In CEL‐treated skin flaps, AMPK inhibitors were demonstrated to suppress the AMPK‐mTOR‐TFEB axis and reduce autophagy levels. This investigation suggests that CEL benefits the survival of RPSF by augmenting angiogenesis and impeding oxidative stress and apoptosis. The results are credited to increased autophagy, made possible by the AMPK‐mTOR‐TFEB axis activation.

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Section: Discussionmentioning

confidence: 99%

Celastrol enhances the viability of random‐pattern skin flaps by regulating autophagy through the AMPK‐mTOR‐TFEB axis

Gu,

Li,

Deng

et al. 2024

Phytotherapy Research

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“…These cells are notably versatile, capable of changing their function in response to stress factors like hypoxia and inflammation, transitioning from a contractile to a secretory state ( 8 ). In this altered state, they release inflammatory cytokines, metalloproteinases, and other substances that contribute to the development of conditions such as atherosclerosis and pulmonary arterial hypertension ( 9 ). Targeting the prevention of VSMC phenotypic transition to preserve their contractile ability offers a promising strategy to slow disease progression.…”

Section: Introductionmentioning

confidence: 99%

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Xin,

Zhang,

et al. 2024

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVD) are the leading cause of death worldwide, despite advances in understanding cardiovascular health. Significant barriers still exist in effectively preventing and managing these diseases. Vascular smooth muscle cells (VSMCs) are crucial for maintaining vascular integrity and can switch between contractile and synthetic functions in response to stimuli such as hypoxia and inflammation. These transformations play a pivotal role in the progression of cardiovascular diseases, facilitating vascular modifications and disease advancement. This article synthesizes the current understanding of the mechanisms and signaling pathways regulating VSMC phenotypic transitions, highlighting their potential as therapeutic targets in cardiovascular disease interventions.

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Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders

Ashique,

Mishra,

Mantry

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Celastrol: The new dawn in the treatment of vascular remodeling diseases

Cited by 6 publications

References 129 publications

Celastrol enhances the viability of random‐pattern skin flaps by regulating autophagy through the AMPK‐mTOR‐TFEB axis

Celastrol enhances the viability of random‐pattern skin flaps by regulating autophagy through the AMPK‐mTOR‐TFEB axis

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders

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