Role of SET7/9 in the progression of ischemic renal injury in diabetic and non-diabetic rats

Sharma, Nisha; Sankrityayan, Himanshu; Kale, Ajinath; Gaikwad, Anil Bhanudas

doi:10.1016/j.bbrc.2020.05.075

Cited by 14 publications

(12 citation statements)

References 33 publications

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“…Our results are in line with previous studies that reported the involvement of Set7 in different models of ischemia. The treatment with Set7 inhibitor improved renal function both in non-diabetic and diabetic rats subjected to ischemic renal injury, indicating that Set7 plays a key role in response to renal ischemia [28]. Likewise, knockdown or inhibition of Set7 in fibroblasts subjected to hypoxia increased the expression of hypoxia-inducible factor target genes, glucose uptake and intracellular adenosine triphosphate levels [27].…”

Section: Discussionmentioning

confidence: 98%

“…Given that obesogenic diet increased Set7 protein levels in the heart of female mice, and that Set7 contributes to ischemia/hypoxia injury [27,28,42,43], we investigated whether Set7 could affect cardiac function following I/R injury in obese female mice. First, baseline cardiac function was evaluated at the stabilization period using the ex vivo Langendorff perfused heart model.…”

Section: Deletion Of Set7 Prevents Cardiac Functional Deterioration A...mentioning

confidence: 99%

“…Several proteins can be methylated by Set7, including estrogen receptor alpha [18], P53 [19], Foxo [20], Akap6 [21], β-catenin [22], Pdx1 [23], Pgc-1α [24], Sirt1 [25], and Nfκb [26]. Functional studies have reported that Set7 affects glucose homeostasis [23,27] and the response to renal ischemic injury [28]. In addition, streptozotocin-induced type 1 diabetic rats have enhanced Set7 protein levels in the heart, suggesting that Set7 may play a role in diabetic cardiomyopathy [29].…”

Section: Introductionmentioning

confidence: 99%

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Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Miranda

Lunardon

Lima

et al. 2022

Cell Physiol Biochem

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Background/Aims: An obesogenic diet (high fat and sugar, low fiber) is associated with an increased risk for metabolic and cardiovascular disorders. Previous studies have demonstrated that epigenetic changes can modify gene transcription and protein function, playing a key role in the development of several diseases. The methyltransferase Set7 methylates histone and non-histone proteins, influencing diverse biological and pathological processes. However, the functional role of Set7 in obesity-associated metabolic and cardiovascular complications is unknown. Methods: Wild type and Set7 knockout female mice were fed a normal diet or an obesogenic diet for 12 weeks. Body weight gain and glucose tolerance were measured. The 3T3-L1 cells were used to determine the role of Set7 in white adipogenic differentiation. Cardiac morphology and function were evaluated by histology and echocardiography. An ex vivo Langendorff perfusion system was used to model cardiac ischemia/reperfusion (I/R). Results: Here, we report that Set7 protein levels were enhanced in the heart and perigonadal adipose tissue (PAT) of female mice fed an obesogenic diet. Significantly, loss of Set7 prevented obesogenic diet-induced glucose intolerance in female mice although it did not affect the obesogenic diet-induced increase in body weight gain and adiposity in these animals, nor did Set7 inhibition change white adipogenic differentiation in vitro. In addition, loss of Set7 prevented the compromised cardiac functional recovery following ischemia and reperfusion (I/R) injury in obesogenic diet-fed female mice; however, deletion of Set7 did not influence obesogenic diet-induced cardiac hypertrophy nor the hemodynamic and echocardiographic parameters. Conclusion: These data indicate that Set7 plays a key role in obesogenic diet-induced glucose intolerance and compromised myocardial functional recovery after I/R in obese female mice.

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Section: Discussionmentioning

confidence: 98%

Section: Deletion Of Set7 Prevents Cardiac Functional Deterioration A...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Miranda

Lunardon

Lima

et al. 2022

Cell Physiol Biochem

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“…In addition to H3K4me2 in the Nrf2 promoter, the methylation of H3K4 by both Set7/9 and stimulated protein-1 (SP1) is enriched in the Keap1 promoter, which promotes the biosynthesis of GSH and regulates oxidative stress in diabetic retinopathy [ 94 ]. Recent findings have revealed that a specific inhibitor of Set7/9, cyproheptadine, alleviates the development of renal ischemia injury in diabetic and nondiabetic rats [ 116 ], indicating that cyproheptadine might be a novel therapeutic agent for diabetic retinopathy. Hyperglycemia induces the Nrf2/Keap1 pathway and the NF- κ B pathway to stimulate the oxidative stress response.…”

Section: Histone Methylation and Oxidative Stress In Cardiovascular D...mentioning

confidence: 99%

Histone Methylation and Oxidative Stress in Cardiovascular Diseases

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Oxidative stress occurs when ROS overproduction overwhelms the elimination ability of antioxidants. Accumulated studies have found that oxidative stress is regulated by histone methylation and plays a critical role in the development and progression of cardiovascular diseases. Targeting the underlying molecular mechanism to alter the interplay of oxidative stress and histone methylation may enable creative and effective therapeutic strategies to be developed against a variety of cardiovascular disorders. Recently, some drugs targeting epigenetic modifiers have been used to treat specific types of cancers. However, the comprehensive signaling pathways bridging oxidative stress and histone methylation need to be deeply explored in the contexts of cardiovascular physiology and pathology before clinical therapies be developed. In the present review, we summarize and update information on the interplay between histone methylation and oxidative stress during the development of cardiovascular diseases such as atherosclerosis, coronary artery disease, pulmonary hypertension, and diabetic macro- and microvascular pathologies.

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“…It is still in its infancy to understand protein methylation in DKD, including its occurence, progression, and treatment. However, research on the connection between histone methylation and non-histone methylation has flourished recently ( 33 ). Below, we summarize studies on the relationship between DKD and protein methylation, including histone methylation and non-histone methylation.…”

Section: Protein Methylation In Diabetic Kidney Diseasementioning

confidence: 99%

Protein Methylation in Diabetic Kidney Disease

et al. 2022

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Chronic kidney disease (CKD) is defined by persistent urine aberrations, structural abnormalities, or impaired excretory renal function. Diabetes is the leading cause of CKD. Their common pathological manifestation is renal fibrosis. Approximately half of all patients with type 2 diabetes and one-third with type 1 diabetes will develop CKD. However, renal fibrosis mechanisms are still poorly understood, especially post-transcriptional and epigenetic regulation. And an unmet need remains for innovative treatment strategies for preventing, arresting, treating, and reversing diabetic kidney disease (DKD). People believe that protein methylation, including histone and non-histone, is an essential type of post-translational modification (PTM). However, prevalent reviews mainly focus on the causes such as DNA methylation. This review will take insights into the protein part. Furthermore, by emphasizing the close relationship between protein methylation and DKD, we will summarize the clinical research status and foresee the application prospect of protein methyltransferase (PMT) inhibitors in DKD treatment. In a nutshell, our review will contribute to a more profound understanding of DKD’s molecular mechanism and inspire people to dig into this field.

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Role of SET7/9 in the progression of ischemic renal injury in diabetic and non-diabetic rats

Cited by 14 publications

References 33 publications

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice

Histone Methylation and Oxidative Stress in Cardiovascular Diseases

Protein Methylation in Diabetic Kidney Disease

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