Vascular autophagy in health and disease

Hughes, William E.; Beyer, Andreas; Gutterman, David D.

doi:10.1007/s00395-020-0802-6

Cited by 63 publications

(51 citation statements)

References 172 publications

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“…During the state of inflammatory stress, endothelial cell function and gene expression switch from a resting to an activated state, contributing to various inflammatory reactions [ 12 ]. Endothelial cells may be affected by inflammatory factors produced by other cells and can also affect the proliferation and contraction of smooth muscle cells through paracrine signaling [ 13 ]. The proliferation of smooth muscle cells is an important feature of late AS development [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

Chang

Zhang

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis is closely associated with the inflammatory reaction of vascular endothelial cells. Puerarin (Pue), the main active component isolated from the rhizome of Pueraria lobata, is an isoflavone compound with potent antioxidant properties. Although Pue exhibits promising antiatherosclerotic pharmacological effects, only a few studies have reported its protective effect on endothelial cells. This study found that Pue could partly regulate mitochondrial function in human umbilical vein endothelial cells (HUVECs) and reduce or inhibit lipopolysaccharide-induced inflammatory reactions and oxidative stress injury in HUVECs, likely via mitochondrial quality control. Furthermore, the protective effect of Pue on HUVECs was closely related to the SIRT-1 signaling pathway. Pue increased autophagy and mitochondrial antioxidant potential via increased SIRT-1 expression, reducing excessive production of ROS and inhibiting the expression of inflammatory factors and oxidative stress injury. Therefore, Pue may improve mitochondrial respiratory function and energy metabolism, increasing the vulnerability of HUVECs to an inflammatory state.

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Section: Introductionmentioning

confidence: 99%

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

Chang

Zhang

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Mitophagy is the selective sequestration of mitochondria by autophagosomes and is degraded by lysosomes to remove damaged mitochondria [ 38 , 39 ]. Excessive mitochondrial fission causes increased mitochondrial debris, resulting in abnormal energy metabolism and apoptotic events.…”

Section: Effects Of Mitochondrial Dynamic Imbalance On the Organismentioning

confidence: 99%

[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Tan

Xia

et al. 2021

Oxidative Medicine and Cellular Longevity

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Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease.

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“…It can therefore be assumed that: (i) a defect in endothelial autophagy enhances pro-atherogenic responses; (ii) the activation of the autophagic flux by adequate shear stress acts as athero-protective mechanism. Enhancing endothelial autophagy within the vasculature might therefore represent a novel and attractive target for the prevention and/or treatment of atherosclerosis and cardiovascular disease (Hughes et al, 2020).…”

Section: Autophagy and The Physiopathology Of Ecsmentioning

confidence: 99%

Autophagy in the Regulation of Tissue Differentiation and Homeostasis

Perrotta

Cattaneo

Molteni

et al. 2020

Front. Cell Dev. Biol.

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Autophagy is a constitutive pathway that allows the lysosomal degradation of damaged components. This conserved process is essential for metabolic plasticity and tissue homeostasis and is crucial for mammalian post-mitotic cells. Autophagy also controls stem cell fate and defective autophagy is involved in many pathophysiological processes. In this review, we focus on established and recent breakthroughs aimed at elucidating the impact of autophagy in differentiation and homeostasis maintenance of endothelium, muscle, immune system, and brain providing a suitable framework of the emerging results and highlighting the pivotal role of autophagic response in tissue functions, stem cell dynamics and differentiation rates.

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Vascular autophagy in health and disease

Cited by 63 publications

References 172 publications

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Autophagy in the Regulation of Tissue Differentiation and Homeostasis

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