<i>N</i>‐acetyl‐seryl‐aspartyl‐lysyl‐proline is a valuable endogenous antifibrotic peptide for kidney fibrosis in diabetes: An update and translational aspects

Kanasaki, Keizo

doi:10.1111/jdi.13219

Cited by 14 publications

(10 citation statements)

References 104 publications

(140 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The Ang1-9 peptide that is increased in COVID-19 BAL stimulates thrombosis by inhibiting fibrinolysis ( Mogielnicki et al, 2014 ). In addition to BK, ACE also degrades the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), which is produced from thymosin beta-4 (TMSB4X, −130 fold) ( Kanasaki, 2020 ). Increased fibrinolysis could therefore be achieved by increasing ACE, or by administering thymosin beta-4, which is currently in clinical trials for the treatment of cardiovascular disorders (Timbetasin).…”

Section: Resultsmentioning

confidence: 99%

A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm

Garvin

Alvarez

Miller

et al. 2020

eLife

353

438

View full text Add to dashboard Cite

Neither the disease mechanism nor treatments for COVID-19 are currently known. Here we present a novel molecular mechanism for COVID-19 that provides therapeutic intervention points that can be addressed with existing FDA-approved pharmaceuticals. The entry point for the virus is ACE2, which is a component of the counteracting hypotensive axis of RAS, that produces the nonapeptide angiotensin1-9 from angiotensin I. Bradykinin is a potent, but often forgotten, part of the vasopressor system that induces hypotension and vasodilation 1, and is regulated by ACE and enhanced by angiotensin1-9 2. Here we perform a completely new analysis on gene expression data from cells of bronchoalveolar lavage samples from COVID-19 patients that were used to sequence the virus, but the host information was discarded 3. Comparison with lavage samples from controls identify a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin (REN) , angiotensin (AGT), key RAS receptors (AGTR2, AGTR1), kinogen (KNG) and the kallikrein enzymes (KLKB1, many of KLK-1-15) that activate it, and both bradykinin receptors (BDKRB1, BDKRB2). This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. These bradykinin-driven outcomes explain many of the symptoms being observed in COVID-19.

show abstract

Section: Resultsmentioning

confidence: 99%

A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm

Garvin

Alvarez

Miller

et al. 2020

eLife

353

438

View full text Add to dashboard Cite

show abstract

“…34 ACE increases fibrinolysis and degrades antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) which is produced from thymosin beta-4. 35…”

Section: Pathophysiology Of Covid-19mentioning

confidence: 99%

Pathophysiology of COVID-19 and its potential therapeutics

Khan

Siddiqui

2021

Int J Basic Clin Pharmacol

View full text Add to dashboard Cite

A series of acute and atypical serious respiratory illnesses were reported in December 2019 from Wuhan, a city of China. It spread to other places and became a global pandemic involving more than 200 countries of the world. Soon, it was discovered that this atypical respiratory illness was caused by a novel corona virus. It was named as the severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) and the disease caused by it as corona virus disease-19 (COVID-19). Since COVID-19 is a new viral disease, world is still struggling to find out a permanent remedy to control this serious health problem. It seems prudent to study or have a look on the pathophysiology of SARS CoV-2 in the light of available research. Further, a review on pathophysiology may give an insight on the potential therapeutic options. Being a new virus and having potential to cause significant morbidity and mortality in short span of time various approved drugs are being repurposed for the treatment of COVID-19.

show abstract

“…Obesity also increases the body's inflammatory response and oxidative stress response, increasing the degree of insulin resistance (2). Kanasaki have proved that obesity, induced by an HFD, is usually accompanied by systemic insulin resistance (IR) (3). The HFD-fed mouse model is considered a reliable model for studying obesity, and related metabolic complications (4).…”

Section: Introductionmentioning

confidence: 99%

Improvement in Mung Bean Peptide on High-Fat Diet-Induced Insulin Resistance Mice Using Untargeted Serum Metabolomics

Tian

Feng

et al. 2022

Front. Nutr.

View full text Add to dashboard Cite

This study aimed to elucidate the potential regulatory mechanism of mung bean peptides (MBPs) on glucolipid metabolism in insulin-resistant mice induced by high-fat diet (HFD) using untargeted serum metabolomics, enzyme linked immunosorbent assay (ELISA), intraperitoneal injection glucose tolerance test (IPGTT), insulin tolerance test (IPITT), and hematoxylin-eosin staining (H&E). The regulatory effect of MBPs for alleviating insulin resistance was studied by measuring body weight, fasting blood glucose (FBG) and serum insulin levels, C-Peptide levels, inflammatory and antioxidant factors, and histopathological observation of C57BL/6 mice. The experimental results showed that dietary intervention with MBPs (245 mg/kg/d) for 5 weeks significantly relieved insulin resistance in HFD mice. The body weight, insulin resistance index, and the levels of FBG, C-Peptide, IL-6, TNF-α, and MDA in the serum of HFD mice significantly decreased (P < 0.05). Conversely, SOD content and pancreatic β cell function index significantly increased (P < 0.05), and the damaged pancreatic tissue was repaired. One biomarker associated with insulin resistance was glycine. In addition, there were four important differential metabolites: pyroglutamate, D-glutamine, aminoadipic acid, and nicotinamide, involved in 12 metabolic pathway changes. It was found that MBPs may regulate amino acid, glycerol phospholipid, fatty acid, alkaloid, and nicotinamide metabolism to regulate the metabolic profile of HFD mice in a beneficial direction.

show abstract

N‐acetyl‐seryl‐aspartyl‐lysyl‐proline is a valuable endogenous antifibrotic peptide for kidney fibrosis in diabetes: An update and translational aspects

Cited by 14 publications

References 104 publications

A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm

A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm

Pathophysiology of COVID-19 and its potential therapeutics

Improvement in Mung Bean Peptide on High-Fat Diet-Induced Insulin Resistance Mice Using Untargeted Serum Metabolomics

Contact Info

Product

Resources

About