Autophagy: an affair of the heart

Gottlieb, Roberta A.; Mentzer, Robert M.

doi:10.1007/s10741-012-9367-2

Cited by 87 publications

(55 citation statements)

References 58 publications

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“…1; * P<0.05 vs. the control group). These findings suggested an enhancement of autophagy in this A/R model and was consistent with a previous finding that autophagy was activated in the heart at baseline and further enhanced during I/R [2] . …”

Section: Activation Of Autophagy In A/rsupporting

confidence: 93%

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Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway

Wang

Cheng

Huang

et al. 2015

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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The purpose of this study was to investigate the potential cardioprotection roles of Rapamycin in anoxia/reoxygenation (A/R) injury of cardiomyocytes through inducing autophagy, and the involvement of PI3k/Akt pathway. We employed simulated A/R of neonatal rat ventricular myocytes (NRVM) as an in vitro model of ischemial/reperfusion (I/R) injury to the heart. NRVM were pretreated with four different concentrations of Rapamycin (20, 50, 100, 150 μmol/L), and pretreated with 10 mmol/L 3-methyladenine (3MA) for inhibiting autophagy during A/R. Then, Western blot analysis was used to examine variation in the expression of LC3-II, LC3-I, Bim, caspase-3, p-PI3KI, PI3KI, p-Akt and Akt. In our model, Rapamycin had a preferential action on autophagy, increasing the expression of LC3-II/LC3-I, whereas decreasing the expression of Bim and caspase-3. Moreover, our results also demonstrated that Rapamycin inhibited the activation of p-PI3KI and enhanced the activation of p-Akt. It is concluded that Rapamycin has a cardioprotection effect by inducing autophagy in a concentration-dependent manner against apopotosis through PI3K/Akt signaling pathway during A/R in NRVM.

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Section: Activation Of Autophagy In A/rsupporting

confidence: 93%

“…Recently, a study showed that autophagy is easily detected under basal condition in heart, and it is further induced during I/R [2] . Autophagy is a dynamic process of intracellular bulk degradation in which cytosolic proteins and organelles are sequestered into double-membrane vesicles, called autophagosomes, to be fused with lysosomes for degradation [3] .…”

mentioning

confidence: 99%

Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway

Wang

Cheng

Huang

et al. 2015

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…Our studies suggest that stimulation of cellular autophagy may also provoke ␤ 2 AR trafficking through autophagosomes. Autophagic activity is augmented in failing hearts (58), but whether this pathway is beneficial or detrimental for cardiomyocyte survival remains controversial (59). Deciphering the relationship between induction of autophagy, trafficking of ␤ARs, and activity of USP20 in healthy versus diseased hearts constitutes an important direction for future research.…”

Section: Discussionmentioning

confidence: 99%

Phosphorylation of the Deubiquitinase USP20 by Protein Kinase A Regulates Post-endocytic Trafficking of β2 Adrenergic Receptors to Autophagosomes during Physiological Stress

Kommaddi

Jean-Charles

Shenoy

2015

Journal of Biological Chemistry

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Background:The mechanisms for recruiting and activating deubiquitinase(s) during GPCR trafficking are unknown. Results: PKA phosphorylation of USP20 Ser-333 inhibits ␤ 2 AR interaction as well as deubiquitination and promotes receptor degradation via autolysosomes during physiological stress. Conclusion: USP20 activity and substrate-specific interaction involves a phosphorylation code. Significance: We identify a novel role for PKA in USP20 regulation and ubiquitin-dependent sorting of GPCRs.

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“…The role of autophagy in I/R injury is controversial [37,38] . In cardiac acute I/R injury, autophagy mediated by AMPactivated protein kinase during ischemia is beneficial, whereas beclin-1-mediated autophagy during reperfusion is detrimental [9] .…”

Section: Discussionmentioning

confidence: 99%

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

et al. 2014

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Aim: Sevoflurane postconditioning (SpostC) has been shown to protect the heart from ischemia-reperfusion (I/R) injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury. Methods: SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% (v/v) sevoflurane during the first 5 min of reperfusion, and chloroquine (10 mg/kg, ip) was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining. Results: I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC. Conclusion: SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues.

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Autophagy: an affair of the heart

Cited by 87 publications

References 58 publications

Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway

Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway

Phosphorylation of the Deubiquitinase USP20 by Protein Kinase A Regulates Post-endocytic Trafficking of β2 Adrenergic Receptors to Autophagosomes during Physiological Stress

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

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