Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways

Li, Chengqiu; Wang, Ting; Zhang, Chunyuan; Xuan, Jichang; Su, C.; Wang, Yuqi

doi:10.1016/j.gene.2015.12.012

Cited by 62 publications

(40 citation statements)

References 38 publications

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“…The reduced starch and seed setting could be explained, at least in part, by an inhibitory effect of glycosidic flavonoids on SS activity, thus disturbing sugar carbon allocation at the sink and source. Flavonoids also inhibit the activity of kinases that control key processes involved in growth and development in animal cells 24, 39 .…”

Section: Discussionmentioning

confidence: 99%

The Sulfoquinovosyltransferase-like Enzyme SQD2.2 is Involved in Flavonoid Glycosylation, Regulating Sugar Metabolism and Seed Setting in Rice

Zhan

Shen

Wang

et al. 2017

Sci Rep

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Seed setting is an important trait that contributes to seed yield and relies greatly on starch accumulation. In this study, a sulfoquinovosyl transferase-like protein, designated as SQD2.2 involved in seed setting and flavonoid accumulation, was identified and characterized in rice. Rice SQD2.2 is localized to the cytoplasm, and the SQD2.2 transcript was highest in leaves. Rice SQD2.2-overexpressing (OE) plants exhibited a decreased seed setting rate and diminished tiller number simultaneously with an increased glycosidic flavonoid level compared with wild-type (WT) plants. SQD2.2 catalyzes the glycosylation of apigenin to produce apigenin 7-O-glucoside using uridine diphosphate-glucose (UDPG) as a sugar donor, but it failed to compensate for sulfoquinovosyldiacylglycerol (SQDG) synthesis in the Arabidopsis sqd2 mutant. Furthermore, apigenin 7-O-glucoside inhibited starch synthase (SS) activity in a concentration-dependent manner, and SQD2.2-OE plants exhibited reduced SS activity accompanied by a significant reduction in starch levels and an elevation in soluble sugar levels relative to WT plants. Both adenosine diphosphate-glucose (ADPG) and UDPG levels in SQD2.2-OE plants were notably lower than those in WT plants. Taken together, rice SQD2.2 exhibits a novel role in flavonoid synthesis and plays an important role in mediating sugar allocation between primary and secondary metabolism in rice.

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Section: Discussionmentioning

confidence: 99%

The Sulfoquinovosyltransferase-like Enzyme SQD2.2 is Involved in Flavonoid Glycosylation, Regulating Sugar Metabolism and Seed Setting in Rice

Zhan

Shen

Wang

et al. 2017

Sci Rep

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“…Although p38 is activated by short repeated cycles of simulated ischemia/reoxygenation termed ischemic preconditioning, preconditioned heart actually exhibited lower p38 activity and was protected against injury during sustained ischemia [90, 91], likely through p38-dependent feedback upregulation of MKP-1 [92]. Inhibition of p38 activity has been proposed as a central mechanism underlying cardioprotection mediated by postconditioning [93], estrogen [94], and quercetin [95]. …”

Section: Mapk Pathwaymentioning

confidence: 99%

Signaling Pathways in Cardiac Myocyte Apoptosis

Xia

Liu

Cheng

2016

BioMed Research International

133

132

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Cardiovascular diseases, the number 1 cause of death worldwide, are frequently associated with apoptotic death of cardiac myocytes. Since cardiomyocyte apoptosis is a highly regulated process, pharmacological intervention of apoptosis pathways may represent a promising therapeutic strategy for a number of cardiovascular diseases and disorders including myocardial infarction, ischemia/reperfusion injury, chemotherapy cardiotoxicity, and end-stage heart failure. Despite rapid growth of our knowledge in apoptosis signaling pathways, a clinically applicable treatment targeting this cellular process is currently unavailable. To help identify potential innovative directions for future research, it is necessary to have a full understanding of the apoptotic pathways currently known to be functional in cardiac myocytes. Here, we summarize recent progress in the regulation of cardiomyocyte apoptosis by multiple signaling molecules and pathways, with a focus on the involvement of these pathways in the pathogenesis of heart disease. In addition, we provide an update regarding bench to bedside translation of this knowledge and discuss unanswered questions that need further investigation.

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“…After hypoxic/ischemic injury, MAPK signaling pathways are activated in the kidney [46][47][48][49] as modulators of ischemia/reperfusion injury. In the past, many studies showed that p38 and JNK are pro-apoptotic, whereas ERKs are the modulators of cell survival under hypoxic/ ischemic conditions [46,[50][51][52][53]. After comprehensively reviewing the literature, however, we believe that the precise changes and roles of MAPK expression and phosphorylation are not that simple.…”

Section: Acute Kidney Injurymentioning

confidence: 99%

Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy

Luo

Shi

et al. 2016

Cell Physiol Biochem

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Tissue hypoxia/ischemia is a pathological feature of many human disorders including stroke, myocardial infarction, hypoxic/ischemic nephropathy, as well as cancer. In the kidney, the combination of limited oxygen supply to the tissues and high oxygen demand is considered the main reason for the susceptibility of the kidney to hypoxic/ischemic injury. In recent years, increasing evidence has indicated that a reduction in renal oxygen tension/blood supply plays an important role in acute kidney injury, chronic kidney disease, and renal tumorigenesis. However, the underlying signaling mechanisms, whereby hypoxia alters cellular behaviors, remain poorly understood. Mitogen-activated protein kinases (MAPKs) are key signal-transducing enzymes activated by a wide range of extracellular stimuli, including hypoxia/ischemia. There are four major family members of MAPKs: the extracellular signal-regulated kinases-1 and -2 (ERK1/2), the c-Jun N-terminal kinases (JNK), p38 MAPKs, and extracellular signal-regulated kinase-5 (ERK5/BMK1). Recent studies, including ours, suggest that these MAPKs are differentially involved in renal responses to hypoxic/ischemic stress. This review will discuss their changes in hypoxic/ischemic pathophysiology with acute kidney injury, chronic kidney diseases and renal carcinoma.

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Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways

Cited by 62 publications

References 38 publications

The Sulfoquinovosyltransferase-like Enzyme SQD2.2 is Involved in Flavonoid Glycosylation, Regulating Sugar Metabolism and Seed Setting in Rice

The Sulfoquinovosyltransferase-like Enzyme SQD2.2 is Involved in Flavonoid Glycosylation, Regulating Sugar Metabolism and Seed Setting in Rice

Signaling Pathways in Cardiac Myocyte Apoptosis

Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy

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