General Information:

Id: 11,717
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Mammalia
review
Reference: Graus-Nunes F and Souza-Mello V(2019) The renin-angiotensin system as a target to solve the riddle of endocrine pancreas homeostasis Biomed. Pharmacother. 109: 639-645 [PMID: 30404071]

Interaction Information:

Comment Obese animals usually showincreased expression of the systemic renin-angiotensin system (RAS)components and show high expression of local RAS elements such asangiotensin-converting enzyme (ACE) and Angiotensin II type I re-ceptor (AT1R) in the pancrea.
Formal Description
Interaction-ID: 116173

disease

Obesity

increases_expression of

gene/protein

ACE

in pancreas
Drugbank entries Show/Hide entries for ACE
Comment Obese animals usually showincreased expression of the systemic renin-angiotensin system (RAS)components and show high expression of local RAS elements such asangiotensin-converting enzyme (ACE) and Angiotensin II type I re-ceptor (AT1R) in the pancrea.
Formal Description
Interaction-ID: 116305

disease

Obesity

increases_expression of

gene/protein

AGTR1

in pancreas
Drugbank entries Show/Hide entries for AGTR1
Comment The local renin-angiotensin system (RAS) in the pancreas modulates glucose-stimulated insulin secretion (GSIS) in beta cells and insulin sensitivity in target tissues.
Formal Description
Interaction-ID: 116307

process

renin-angiotensin system

affects_activity of

in pancreas
Comment The local renin-angiotensin system (RAS) in the pancreas modulates glucose-stimulated insulin secretion (GSIS) in beta cells and insulin sensitivity in target tissues.
Formal Description
Interaction-ID: 116315

process

renin-angiotensin system

affects_activity of

Comment Angiotensinogen is the substrate for renin and is mainly expressed in the alpha cells, which secrete the hormone glucagon.
Formal Description
Interaction-ID: 116318

gene/protein

AGT

is_expressed_in

tissue/cell line

pancreatic alpha cell

Comment ACE is responsible for the conversion of angiotensin 1 into angiotensin 2 and is mainly expressed in the islet periphery and in its microvasculature.
Formal Description
Interaction-ID: 116319

gene/protein

ACE

decreases_quantity of

gene/protein

Angiotensin I

Drugbank entries Show/Hide entries for ACE
Comment ACE is responsible for the conversion of angiotensin 1 into angiotensin 2 and is mainly expressed in the islet periphery and in its microvasculature.
Formal Description
Interaction-ID: 116323

gene/protein

ACE

increases_quantity of

gene/protein

Angiotensin II

Drugbank entries Show/Hide entries for ACE
Comment The angiotensin 2 (ANG2) receptors are found within the islet, and AT1R is mainly found in the islet core where the beta cells responsible for insulin secretion are located. The angiotensin II type 2 receptor (AT2R) is found in nearby delta cells that secrete somatostatin. Angiotensin-convertingenzyme 2 (ACE2) is expressed by alpha cells and the islet micro-vasculature, though the latter is more implicated in glycemic homeostasis and islet maintenance.
Formal Description
Interaction-ID: 116324

gene/protein

AGTR1

is_expressed_in

tissue/cell line

pancreatic islet

Drugbank entries Show/Hide entries for AGTR1
Comment The angiotensin 2 (ANG2) receptors are found within the islet, and AT1R is mainly found in the islet core where the beta cells responsible for insulin secretion are located. The angiotensin II type 2 receptor (AT2R) is found in nearby delta cells that secrete somatostatin. Angiotensin-convertingenzyme 2 (ACE2) is expressed by alpha cells and the islet micro-vasculature, though the latter is more implicated in glycemic homeostasis and islet maintenance.
Formal Description
Interaction-ID: 116329

gene/protein

AGTR2

is_expressed_in

tissue/cell line

pancreatic islet

Drugbank entries Show/Hide entries for AGTR2
Comment The angiotensin 2 (ANG2) receptors are found within the islet, and AT1R is mainly found in the islet core where the beta cells responsible for insulin secretion are located. The angiotensin II type 2 receptor (AT2R) is found in nearby delta cells that secrete somatostatin. Angiotensin-convertingenzyme 2 (ACE2) is expressed by alpha cells and the islet micro-vasculature, though the latter is more implicated in glycemic homeostasis and islet maintenance.
Formal Description
Interaction-ID: 116331

gene/protein

ACE2

is_expressed_in

tissue/cell line

pancreatic islet

Drugbank entries Show/Hide entries for ACE2
Comment The insulin-resistant state causes high expression of AT1R in the pancreas.
Formal Description
Interaction-ID: 116333

disease

Insulin resistance

increases_expression of

gene/protein

AGTR1

in pancreas
Drugbank entries Show/Hide entries for AGTR1
Comment Intra-islet AT1R upregulation reduces islet bloodflow and (pro) insulin synthesis, both of which impair GSIS. Moreover, excessive AT1R expression by the hypertrophied beta cells enhances oxidative stress and favors apoptosis and fibrosis. These changes cause beta cell dysfunction and diminish islet lifespan.
Formal Description
Interaction-ID: 116335

gene/protein

AGTR1

decreases_activity of

process

proinsulin synthesis

in pancreas
Drugbank entries Show/Hide entries for AGTR1
Comment Intra-islet AT1R upregulation reduces islet bloodflow and (pro) insulin synthesis, both of which impair GSIS. Moreover, excessive AT1R expression by the hypertrophied beta cells enhances oxidative stress and favors apoptosis and fibrosis. These changes cause beta cell dysfunction and diminish islet lifespan.
Formal Description
Interaction-ID: 116341

gene/protein

AGTR1

increases_activity of

in pancreas
Drugbank entries Show/Hide entries for AGTR1
Comment Intra-islet AT1R upregulation reduces islet bloodflow and (pro) insulin synthesis, both of which impair GSIS. Moreover, excessive AT1R expression by the hypertrophied beta cells enhances oxidative stress and favors apoptosis and fibrosis. These changes cause beta cell dysfunction and diminish islet lifespan.
Formal Description
Interaction-ID: 116343

gene/protein

AGTR1

increases_activity of

in pancreas
Drugbank entries Show/Hide entries for AGTR1
Comment Intra-islet AT1R upregulation reduces islet bloodflow and (pro) insulin synthesis, both of which impair GSIS. Moreover, excessive AT1R expression by the hypertrophied beta cells enhances oxidative stress and favors apoptosis and fibrosis. These changes cause beta cell dysfunction and diminish islet lifespan.
Formal Description
Interaction-ID: 116345

gene/protein

AGTR1

increases_activity of

phenotype

pancreas fibrosis

Drugbank entries Show/Hide entries for AGTR1
Comment The ACE2/MAS receptor axis converts angiotensin 2 (ANG2) to ANG1-7 and counters the harmful effects caused by the interaction of ANG2 with the AT1R.
Formal Description
Interaction-ID: 116346

gene/protein

ACE2

decreases_quantity of

gene/protein

Angiotensin II

Drugbank entries Show/Hide entries for ACE2
Comment The ACE2/MAS receptor axis converts angiotensin 2 (ANG2) to ANG1-7 and counters the harmful effects caused by the interaction of ANG2 with the AT1R.
Formal Description
Interaction-ID: 116348

gene/protein

ACE2

increases_quantity of

gene/protein

Angiotensin (1-7)

Drugbank entries Show/Hide entries for ACE2
Comment ANG1-7 has an important role in the regulation of insulin secretion in mouse islets both in vitro and in vivo by controlling MAS receptor-dependent signaling.
Formal Description
Interaction-ID: 116350

gene/protein

Angiotensin (1-7)

affects_activity of

Comment ANG1-7 has an important role in the regulation of insulin secretion in mouse islets both in vitro and in vivo by controlling MAS receptor-dependent signaling.
Formal Description
Interaction-ID: 116374

gene/protein

Angiotensin (1-7)

affects_activity of

gene/protein

MAS1

Comment ANG1-7 has an important role in the regulation of insulin secretion in mouse islets both in vitro and in vivo by controlling MAS receptor-dependent signaling. The effects of the ANG1-7-dependent MAS receptor are not linked to insulin excitation-secretion coupling alterations. However, the intracellular increase in cAMP modulates the accessory pathway promoting an improvement in insulin secretion.
Formal Description
Interaction-ID: 116377

gene/protein

Angiotensin (1-7)

increases_quantity of

drug/chemical compound

cAMP

in the cell
Drugbank entries Show/Hide entries for cAMP
Comment There is increased islet vascularization observed in obese subjects, and this could be a compensatory response to support the augmented beta cell mass due to islet hypertrophy. If ACE2 deletion occurs, then the vascular compensation in the islets is reduced.
Formal Description
Interaction-ID: 116380

disease

Obesity

increases_activity of

phenotype

increased pancreatic islet vascularization

Comment There is increased islet vascularization observed in obese subjects, and this could be a compensatory response to support the augmented beta cell mass due to islet hypertrophy. If ACE2 deletion occurs, then the vascular compensation in the islets is reduced.
Formal Description
Interaction-ID: 116381

gene/protein

ACE2

affects_activity of

phenotype

increased pancreatic islet vascularization

Drugbank entries Show/Hide entries for ACE2
Comment Reduced ACE2 expression in islet endothelial cells rather than in islet cells themselves leads to a decreased tolerance to glucose and impaired GSIS.
Formal Description
Interaction-ID: 116382
Drugbank entries Show/Hide entries for ACE2
Comment Losartan and telmisartan (two widelyprescribed ARBs) were recently shown to mitigate islet hypertrophy while increasing islet vascularization in diet-induced obese C57BL/6mice. These results suggest that ACE2/ANG1-7 was favored by the selective inhibition of ANG2 interaction with AT1R.
Formal Description
Interaction-ID: 116383

drug/chemical compound

Losartan

increases_activity of

Drugbank entries Show/Hide entries for Losartan
Comment Losartan and telmisartan (two widelyprescribed ARBs) were recently shown to mitigate islet hypertrophy while increasing islet vascularization in diet-induced obese C57BL/6mice. These results suggest that ACE2/ANG1-7 was favored by the selective inhibition of ANG2 interaction with AT1R.
Formal Description
Interaction-ID: 116384

drug/chemical compound

Telmisartan

increases_activity of

Drugbank entries Show/Hide entries for Telmisartan
Comment Losartan and telmisartan (two widelyprescribed ARBs) were recently shown to mitigate islet hypertrophy while increasing islet vascularization in diet-induced obese C57BL/6mice. These results suggest that ACE2/ANG1-7 was favored by the selective inhibition of ANG2 interaction with AT1R.
Formal Description
Interaction-ID: 116386

drug/chemical compound

Losartan

increases_activity of

phenotype

increased pancreatic islet vascularization

Drugbank entries Show/Hide entries for Losartan
Comment Losartan and telmisartan (two widelyprescribed ARBs) were recently shown to mitigate islet hypertrophy while increasing islet vascularization in diet-induced obese C57BL/6mice. These results suggest that ACE2/ANG1-7 was favored by the selective inhibition of ANG2 interaction with AT1R.
Formal Description
Interaction-ID: 116387

drug/chemical compound

Telmisartan

increases_activity of

phenotype

increased pancreatic islet vascularization

Drugbank entries Show/Hide entries for Telmisartan
Comment The reduction or impairment of ACE2 functioning, which is responsible for cleaving ANG2 to ANG (1-7), contributes to islet dysfunction and to T2DM due to impaired beta cell proliferation and the resulting reduced beta cell mass.
Formal Description
Interaction-ID: 116389

gene/protein

ACE2

affects_activity of

Drugbank entries Show/Hide entries for ACE2
Comment The reduction or impairment of ACE2 functioning, which is responsible for cleaving ANG2 to ANG (1-7), contributes to islet dysfunction and to T2DM due to impaired beta cell proliferation and the resulting reduced beta cell mass.
Formal Description
Interaction-ID: 116390

gene/protein

ACE2

affects_activity of

Drugbank entries Show/Hide entries for ACE2
Comment The infusion of ANG2 in mice causes hyperglycemia and hyperinsulinemia coupled with decreased GSIS.
Formal Description
Interaction-ID: 116391

gene/protein

Angiotensin II

increases_activity of

phenotype

hyperglycemia

Comment The infusion of ANG2 in mice causes hyperglycemia and hyperinsulinemia coupled with decreased GSIS.
Formal Description
Interaction-ID: 116394

gene/protein

Angiotensin II

increases_activity of

Comment Decreased ACE2 expression and activity stimulate a compensatory increase in AT1R expression and result in enhanced oxidative stress in the pancreas.
Formal Description
Interaction-ID: 116395

gene/protein

ACE2

affects_expression of

gene/protein

AGTR1

in pancreas
Drugbank entries Show/Hide entries for ACE2 or AGTR1
Comment Decreased ACE2 expression and activity stimulate a compensatory increase in AT1R expression and result in enhanced oxidative stress in the pancreas.
Formal Description
Interaction-ID: 116396

gene/protein

ACE2

affects_activity of

in pancreas
Drugbank entries Show/Hide entries for ACE2
Comment Renin represents a key point for the complete inhibition of the RAS cascade. Renin expression in the islet was increased by aliskiren due to a feedback mechanism activated by the inhibition of plasma renin activity. Aliskiren directly promotes the inhibition of renin and exerts a beneficial effect on glucose intolerance and pancreatic damage in experimental diabetes models through the attenuation of oxidative stress.
Formal Description
Interaction-ID: 116397

gene/protein

REN

increases_activity of

process

renin-angiotensin system

Drugbank entries Show/Hide entries for REN
Comment Renin represents a key point for the complete inhibition of the RAS cascade. Renin expression in the islet was increased by aliskiren due to a feedback mechanism activated by the inhibition of plasma renin activity. Aliskiren directly promotes the inhibition of renin and exerts a beneficial effect on glucose intolerance and pancreatic damage in experimental diabetes models through the attenuation of oxidative stress.
Formal Description
Interaction-ID: 116400

drug/chemical compound

Aliskiren

decreases_activity of

gene/protein

REN

Drugbank entries Show/Hide entries for Aliskiren or REN
Comment Renin represents a key point for the complete inhibition of the RAS cascade. Renin expression in the islet was increased by aliskiren due to a feedback mechanism activated by the inhibition of plasma renin activity. Aliskiren directly promotes the inhibition of renin and exerts a beneficial effect on glucose intolerance and pancreatic damage in experimental diabetes models through the attenuation of oxidative stress.
Formal Description
Interaction-ID: 116401

drug/chemical compound

Aliskiren

decreases_activity of

Drugbank entries Show/Hide entries for Aliskiren
Comment Renin represents a key point for the complete inhibition of the RAS cascade. Renin expression in the islet was increased by aliskiren due to a feedback mechanism activated by the inhibition of plasma renin activity. Aliskiren directly promotes the inhibition of renin and exerts a beneficial effect on glucose intolerance and pancreatic damage in experimental diabetes models through the attenuation of oxidative stress.
Formal Description
Interaction-ID: 116402

drug/chemical compound

Aliskiren

decreases_activity of

Drugbank entries Show/Hide entries for Aliskiren
Comment Increased intra-islet RAS activity is associated with oxidative stress, which damages endoplasmic reticulum (ER) function. ER stress and the subsequent beta cell dysfunction were attenuated by renin inhibition with aliskiren in Ren2 rats by the correction of mitochondrial abnormalities, normalization of reactive oxygen species levels and reestablishment of the intra-islet insulin signaling cascade.
Formal Description
Interaction-ID: 116403

drug/chemical compound

Aliskiren

decreases_activity of

in pancreatic islets
Drugbank entries Show/Hide entries for Aliskiren
Comment Increased intra-islet RAS activity is associated with oxidative stress, which damages endoplasmic reticulum (ER) function. ER stress and the subsequent beta cell dysfunction were attenuated by renin inhibition with aliskiren in Ren2 rats by the correction of mitochondrial abnormalities, normalization of reactive oxygen species levels and reestablishment of the intra-islet insulin signaling cascade.
Formal Description
Interaction-ID: 116404

drug/chemical compound

Aliskiren

increases_activity of

in pancreatic islets
Drugbank entries Show/Hide entries for Aliskiren
Comment Patients with pre-diabetes and diabetes benefited from ACE inhibition and showed reduced islet inflammation and an improved ACE2 axis.
Formal Description
Interaction-ID: 116405

drug/chemical compound

ACE inhibitor

decreases_activity of

in pancreatic islets
Comment Patients with pre-diabetes and diabetes benefited from ACE inhibition and showed reduced islet inflammation and an improved ACE2 axis.
Formal Description
Interaction-ID: 116407

drug/chemical compound

ACE inhibitor

increases_activity of

gene/protein

ACE2

in pancreatic islets
Drugbank entries Show/Hide entries for ACE2
Comment Mitochondrial metabolism plays an important role in the release of insulin and glucose homeostasis. Evidence shows that overexpression of ACE2 can regulate mitochondrial function in pancreatic beta cells and restore GSIS.
Formal Description
Interaction-ID: 116408

gene/protein

ACE2

increases_activity of

cellular component

mitochondrion

in pancreatic beta cells
Drugbank entries Show/Hide entries for ACE2
Comment ANG2 interaction with AT1R leads to vasoconstriction, cell growth, inflammation, fibrosis and oxidative stress.
Formal Description
Interaction-ID: 116409

gene/protein

Angiotensin II

increases_activity of

gene/protein

AGTR1

Drugbank entries Show/Hide entries for AGTR1
Comment ANG2 interaction with AT1R leads to vasoconstriction, cell growth, inflammation, fibrosis and oxidative stress.
Formal Description
Interaction-ID: 116410

gene/protein

AGTR1

increases_activity of

Drugbank entries Show/Hide entries for AGTR1
Comment ANG2 interaction with AT1R leads to vasoconstriction, cell growth, inflammation, fibrosis and oxidative stress.
Formal Description
Interaction-ID: 116411

gene/protein

AGTR1

increases_activity of

Drugbank entries Show/Hide entries for AGTR1
Comment ANG2 interaction with AT1R leads to vasoconstriction, cell growth, inflammation, fibrosis and oxidative stress.
Formal Description
Interaction-ID: 116412

gene/protein

AGTR1

increases_activity of

phenotype

pancreas fibrosis

Drugbank entries Show/Hide entries for AGTR1
Comment ANG2 interaction with AT1R leads to vasoconstriction, cell growth, inflammation, fibrosis and oxidative stress.
Formal Description
Interaction-ID: 116413

gene/protein

AGTR1

increases_activity of

Drugbank entries Show/Hide entries for AGTR1
Comment AT2R is involved in vasodilatation and regulates pancreas development.
Formal Description
Interaction-ID: 116414

gene/protein

AGTR2

increases_activity of

process

vasodilation

Drugbank entries Show/Hide entries for AGTR2
Comment AT2R is involved in vasodilatation and regulates pancreas development. Considering that hyperglycemia causes AT2R downregulation, this might be a promising target for treatment or prevention of T2DM by stimulating beta-cell neogenesis.
Formal Description
Interaction-ID: 116415

phenotype

hyperglycemia

decreases_expression of

gene/protein

AGTR2

Drugbank entries Show/Hide entries for AGTR2
Comment The intra-islet AT1R expression level is a master regulator of beta cell sensitivity to insulin. Therefore, it influences glucose-induced insulin and glucagon release.
Formal Description
Interaction-ID: 116416
Drugbank entries Show/Hide entries for AGTR1
Comment The intra-islet AT1R expression level is a master regulator of beta cell sensitivity to insulin. Therefore, it influences glucose-induced insulin and glucagon release.
Formal Description
Interaction-ID: 116417

gene/protein

AGTR1

affects_activity of

Drugbank entries Show/Hide entries for AGTR1
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116418

gene/protein

AGTR1

affects_expression of

gene/protein

IRS1

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or IRS1
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116419

gene/protein

AGTR1

affects_expression of

gene/protein

IRS2

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116420

gene/protein

AGTR1

affects_expression of

complex/PPI

Phosphatidylinositol 3-kinase

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116421

gene/protein

AGTR1

affects_expression of

gene/protein

AKT2

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or AKT2
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116422

gene/protein

AGTR1

affects_activity of

gene/protein

SLC2A2

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or SLC2A2
Comment The selective blockade of intra-islet AT1R caused in-creased insulin receptor substrate (IRS) - 1 (IRS-1), IRS-2, phosphoinositide 3-kinase (PI3K), and phospho-protein kinase B (AKT) 2 expression levels. Additionally, there were increased activities of the glucose-sensing apparatus such as GLUT-2 and glucokinase (GCK) in pancreatic islets.
Formal Description
Interaction-ID: 116423

gene/protein

AGTR1

affects_activity of

gene/protein

GCK

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or GCK
Comment ANG2 interaction with AT1R impairs glucose metabolism through inflammatory signals mediated by the high expression of interleukin-1beta (IL-1beta) and nuclear factor-kappaB (NF-kappaB) coupled with inducible nitric oxide synthase (iNOS) in pancreatic islets.
Formal Description
Interaction-ID: 116424

gene/protein

AGTR1

increases_expression of

gene/protein

IL1B

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or IL1B
Comment ANG2 interaction with AT1R impairs glucose metabolism through inflammatory signals mediated by the high expression of interleukin-1beta (IL-1beta) and nuclear factor-kappaB (NF-kappaB) coupled with inducible nitric oxide synthase (iNOS) in pancreatic islets.
Formal Description
Interaction-ID: 116425

gene/protein

AGTR1

increases_activity of

complex/PPI

NF-kappaB complex

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1
Comment ANG2 interaction with AT1R impairs glucose metabolism through inflammatory signals mediated by the high expression of interleukin-1beta (IL-1beta) and nuclear factor-kappaB (NF-kappaB) coupled with inducible nitric oxide synthase (iNOS) in pancreatic islets.
Formal Description
Interaction-ID: 116426

gene/protein

AGTR1

increases_expression of

gene/protein

NOS2

in pancreatic islets
Drugbank entries Show/Hide entries for AGTR1 or NOS2
Comment AT1R blockade by valsartan decreased islet hypertrophy, enhanced mitochondrial activity, decreased interferon gamma expression, and mildly enhanced insulin secretion in islets.
Formal Description
Interaction-ID: 116427

drug/chemical compound

Valsartan

decreases_activity of

gene/protein

AGTR1

Drugbank entries Show/Hide entries for Valsartan or AGTR1
Comment AT1R blockade by valsartan decreased islet hypertrophy, enhanced mitochondrial activity, decreased interferon gamma expression, and mildly enhanced insulin secretion in islets.
Formal Description
Interaction-ID: 116428

drug/chemical compound

Valsartan

decreases_activity of

Drugbank entries Show/Hide entries for Valsartan
Comment AT1R blockade by valsartan decreased islet hypertrophy, enhanced mitochondrial activity, decreased interferon gamma expression, and mildly enhanced insulin secretion in islets.
Formal Description
Interaction-ID: 116429

drug/chemical compound

Valsartan

increases_activity of

cellular component

mitochondrion

in pancreatic islets
Drugbank entries Show/Hide entries for Valsartan
Comment AT1R blockade by valsartan decreased islet hypertrophy, enhanced mitochondrial activity, decreased interferon gamma expression, and mildly enhanced insulin secretion in islets.
Formal Description
Interaction-ID: 116430

drug/chemical compound

Valsartan

decreases_expression of

gene/protein

IFNG

in pancreatic islets
Drugbank entries Show/Hide entries for Valsartan or IFNG
Comment AT1R blockade by valsartan decreased islet hypertrophy, enhanced mitochondrial activity, decreased interferon gamma expression, and mildly enhanced insulin secretion in islets.
Formal Description
Interaction-ID: 116431

drug/chemical compound

Valsartan

increases_activity of

in pancreatic islets
Drugbank entries Show/Hide entries for Valsartan
Comment Osteoprotegerin (OPG) is a protein that is homologous to the tumor necrosis factor (TNF) receptors and favors the increase in monocyte/macrophage infiltration, fibrosis and apoptosis that reduces islet function in diabetic mice. OPG induces a significant increase in the ACE and AT1R gene and protein expression, and the molecular mechanism maybe linked to activation of the mitogen-activated protein kinase (MAPK) and NF-kappaB transduction pathways.
Formal Description
Interaction-ID: 116432

gene/protein

TNFRSF11B

increases_expression of

gene/protein

ACE

Drugbank entries Show/Hide entries for ACE
Comment Osteoprotegerin (OPG) is a protein that is homologous to the tumor necrosis factor (TNF) receptors and favors the increase in monocyte/macrophage infiltration, fibrosis and apoptosis that reduces islet function in diabetic mice. OPG induces a significant increase in the ACE and AT1R gene and protein expression, and the molecular mechanism maybe linked to activation of the mitogen-activated protein kinase (MAPK) and NF-kappaB transduction pathways.
Formal Description
Interaction-ID: 116433

gene/protein

TNFRSF11B

increases_expression of

gene/protein

AGTR1

Drugbank entries Show/Hide entries for AGTR1
Comment Oxidative stress is pivotal for beta cell loss. ANG (1-7) treatment reduced ROS generation by improving mitochondrial function ina n in vitro model of oxidative stress using INS-1 cells.
Formal Description
Interaction-ID: 116434

gene/protein

Angiotensin (1-7)

decreases_activity of

Comment Neprilysin is a highly expressed islet peptidase that degrades ANG(1-7) to several peptides.
Formal Description
Interaction-ID: 116435

gene/protein

MME

decreases_quantity of

gene/protein

Angiotensin (1-7)

Drugbank entries Show/Hide entries for MME