Nobiletin attenuates adverse cardiac remodeling after acute myocardial infarction in rats via restoring autophagy flux

Wu, Xiaoqian; Zheng, Dechong; Qin, Yuyan; Liu, Zumei; Zhang, Guiping; Zhu, Xiaoyan; Zeng, Li-Huan; Liang, Zhenye

doi:10.1016/j.bbrc.2017.08.064

Cited by 51 publications

(36 citation statements)

References 26 publications

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“…5-7g). 3-MA permanently inhibits type I PI3K but transiently impedes type III PI3K, thus mainly inhibiting autophagosome formation 27 . This finding may explain why 3-MA alleviated LC3-II accumulation induced by Cd and significantly inhibited autophagosome formation in GC-2/TM3/TM4 cells.…”

Section: Discussionmentioning

confidence: 99%

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Wang

et al. 2020

Cell Death Dis

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Autophagy and apoptosis are two major modes of cell death. A balanced interplay between both is vital for phagocytic clearance of apoptotic testicular cells. Here, generating a SD rats model-treated with cadmium (Cd) to mimic environmental exposure on human, we show that autophagy and apoptosis present synchronous change trends in Cd-induced testicular injury/self-recovery. Further, the cross-talk of autophagy and apoptosis is investigated in four testicular cell lines (GC-1/GC-2/TM3/TM4 cells) respectively. Results reveal that Cd-exposure for five consecutive weeks induces reproductive toxicity in male rats. After one cycle of spermatogenesis within 8 weeks without Cd, toxic effects are ameliorated significantly. In vitro, we find that PI3K inhibitor 3-MA regulates apoptosis by inhibiting autophagy with mTOR-independent pathway in Cd-treated testicular cells. Conclusively, cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by Cd via PI3K with mTOR-independent pathway.

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Section: Discussionmentioning

confidence: 99%

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Wang

et al. 2020

Cell Death Dis

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“…Cells were plated on a confocal plate and infected with adenovirus HBAD-mRFP-GFP-LC3 with 250 (multiplicity of infection, MOI) (Wu et al, 2017). Procedures are stated in Supplementary data.…”

Section: Transfection Of Adenovirus Hbad-mrfp-gfp-lc3/gfp-lc3mentioning

confidence: 99%

“…This compensatory activation is able to mitigate energy loss and clean damaged mitochondria and protein aggregates (Yan et al, 2005;Hongxin et al, 2007). Taking acute myocardial infarction as an example, most previous studies report that autophagy is activated in the border zone of acute MI (Chiang et al, 2017;Wu et al, 2017); however, the impaired proteins and organelles, formed as aggresomes, and/or the autophagic degradation-related protein p62 are still largely accumulated, suggesting insufficient clearance by autophagy. This is consistent with our finding that autophagy marker LC3 II, together with upstream factors (AMPK, Beclin1, ULK, etc.)…”

Section: Ubc9 and Autophagic Flux Regulationmentioning

confidence: 99%

Ubc9 Attenuates Myocardial Ischemic Injury Through Accelerating Autophagic Flux

et al. 2020

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“…Autophagy and the inflammatory response can be activated after AMI. 21 , 22 , 23 Autophagy is a homeostatic process that can prevent damage to healthy cells. However, sustained autophagy can lead to cell death in an emergency situation.…”

Section: Introductionmentioning

confidence: 99%

miR-93-5p-Containing Exosomes Treatment Attenuates Acute Myocardial Infarction-Induced Myocardial Damage

Liu

Jiang

Deng

et al. 2018

Molecular Therapy - Nucleic Acids

159

114

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Adipose-derived stromal cells (ADSCs) have been considered as an attractive therapeutic tool. Accumulating evidence indicates that the healing effects of ADSCs are mainly related to paracrine action rather than transdifferentiation. Data show that the expression of miR-93-5p has a cardio-protective effect after acute myocardial infarction (AMI). To identify whether miR-93-5p-encapsulating exosomes that form ADSCs have a better cardio-protective effect, we investigated the inflammatory factors and miR-30d-5p expression in clinical levels. A rat model of AMI and an in vitro model of hypoxic H9c2 cells were established to study the protective mechanism of miR-93-5p in ischemia-induced cardiac injury. The results show that the expression of inflammatory cytokines and miR-93-5p were increased following AMI in both patients and animal models. Moreover, treatment with ADSC-derived miR-93-5p-containing exosomes has a greater protective effect on infarction-induced myocardial damage than simple exosome processing. Furthermore, in vitro experiments confirmed that the expression of miR-93-5p can significantly suppress hypoxia-induced autophagy and inflammatory cytokine expression by targeting Atg7 and Toll-like receptor 4 (TLR4), respectively, and was confirmed with Atg7 or TLR4 overexpression. The results also show that autophagy activation can promote inflammatory cytokine expression indirectly. Taken together, these results suggest that the miR-93-5p-enhanced ADSC-derived exosomes prevent cardiac injury by inhibiting autophagy and the inflammatory response.

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Nobiletin attenuates adverse cardiac remodeling after acute myocardial infarction in rats via restoring autophagy flux

Cited by 51 publications

References 26 publications

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Ubc9 Attenuates Myocardial Ischemic Injury Through Accelerating Autophagic Flux

miR-93-5p-Containing Exosomes Treatment Attenuates Acute Myocardial Infarction-Induced Myocardial Damage

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