Potential of Polyphenols to Restore SIRT1 and NAD+ Metabolism in Renal Disease DOI Open Access
Claudia Tovar‐Palacio, Lilia G. Noriega, Adriana Mercado

et al.

Nutrients, Journal Year: 2022, Volume and Issue: 14(3), P. 653 - 653

Published: Feb. 3, 2022

SIRT1 is an NAD+-dependent class III histone deacetylase that abundantly expressed in the kidney, where it modulates gene expression, apoptosis, energy homeostasis, autophagy, acute stress responses, and mitochondrial biogenesis. Alterations activity NAD+ metabolism are frequently observed chronic kidney diseases of diverse origins, including obesity diabetes. Nevertheless, vitro vivo studies clinical trials with humans show SIRT1-activating compounds derived from natural sources, such as polyphenols found fruits, vegetables, plants, resveratrol, quercetin, isoflavones, can prevent disease be part treatments for a wide variety diseases. Here, we summarize roles renal pathophysiology provide overview have potential to restore

Language: Английский

Role of the renin–angiotensin system in the pathophysiology of coronary heart disease and heart failure: Diagnostic biomarkers and therapy with drugs and natural products DOI Creative Commons

Jinit K. Mehta,

Ginpreet Kaur, Harpal S. Buttar

et al.

Frontiers in Physiology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 23, 2023

The renin–angiotensin system (RAS) plays a pivotal role in blood pressure regulation. In some cases, this steering mechanism is affected by various deleterious factors (mainly via the overactivation of RAS) causing cardiovascular damage, including coronary heart disease (CHD) that can ultimately lead to chronic failure (CHF). This not only causes disability and absenteeism from work but also imposes significant healthcare costs globally. incidence diseases has escalated exponentially over years with major outcome form CHD, stroke, CHF. involvement RAS been extensively researched limelight on CHD. may trigger cascade events atherosclerotic mayhem, which CHD related aggravation damaging endothelial lining vessels inflammatory oxidative stress pathways. Although there are diagnostic tests treatments available market, constant need for development procedures therapeutic strategies increase patient compliance reduce associated side effects. review highlights advances treatment domains would help subjugating effects caused conventional therapy.

Language: Английский

Citations

22

Ellagic acid ameliorates aging-induced renal oxidative damage through upregulating SIRT1 and NRF2 DOI Creative Commons
Niloufar Naghibi, Asie Sadeghi, Sajjadeh Movahedinia

et al.

BMC Complementary Medicine and Therapies, Journal Year: 2023, Volume and Issue: 23(1)

Published: March 10, 2023

Abstract Background Aging is associated with impaired renal function and structural alterations. Oxidative stress plays a vital role in senescence damage. Sirtuin 1 (SIRT1) thought to protect cells from oxidative through nuclear factor erythroid 2-related 2 (NRF2). Ellagic acid (EA), natural antioxidant, has been demonstrated have renoprotective roles vitro vivo. This study investigated if SIRT1 NRF2 mediate the protective effects of EA aged kidneys. Methods Male Wistar rats were divided into three groups including young (4 months), old, old + (25 months). Young received solvent, while group was treated (30 mg/kg) by gavage for 30 days. Then, level stress, expression, kidney parameters, histopathological indices measured. Results Treatment significantly increased antioxidant enzymes reduced malondialdehyde concentration ( P < 0.01). Moreover, administration remarkably upregulated mRNA protein levels as well deacetylated 0.05). Additionally, improved scores Conclusions These findings suggest that ellagic exerts on kidneys activating signaling.

Language: Английский

Citations

22

Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19 DOI Creative Commons
Cameron D. Owens, Camila Bonin Pinto,

Sam Detwiler

et al.

Brain Communications, Journal Year: 2024, Volume and Issue: 6(2)

Published: Jan. 1, 2024

Abstract Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds infection) alter cellular physiologic processes within the neurovascular unit contribute cognitive dysfunction. COVID-19 has posed significant complications during acute convalescent stages in multiple organ systems, including brain. Cognitive impairment is prevalent complication patients, irrespective of severity SARS-CoV-2 infection. Moreover, overwhelming evidence from vitro, preclinical clinical studies reported SARS-CoV-2-induced pathologies components are associated with impairment. Neurovascular disruption alters coupling response, critical mechanism regulates cerebromicrovascular blood flow meet energetic demands locally active neurons. Normal processing achieved through response involves coordinated action cells (i.e. neurons glia) cell types endothelia, smooth muscle pericytes). However, current work on COVID-19-induced yet investigate as causal factor. Hence, this review, we aim describe SARS-CoV-2's effects how they can impact decline disease. Additionally, explore potential therapeutic interventions mitigate Given great both individuals public health, necessity effort fundamental scientific research application becomes imperative. This integrated endeavour crucial mitigating deficits induced by its subsequent burden especially vulnerable population.

Language: Английский

Citations

10

Can phytotherapy with polyphenols serve as a powerful approach for the prevention and therapy tool of novel coronavirus disease 2019 (COVID-19)? DOI Open Access
Émile Lévy,

Edgard Delvin,

Valérie Marcil

et al.

AJP Endocrinology and Metabolism, Journal Year: 2020, Volume and Issue: 319(4), P. E689 - E708

Published: Aug. 5, 2020

Much more serious than the previous severe acute respiratory syndrome (SARS) coronavirus (CoV) outbreaks, novel SARS-CoV-2 infection has spread speedily, affecting 213 countries and causing ∼17,300,000 cases ∼672,000 (∼+1,500/day) deaths globally (as of July 31, 2020). The potentially fatal disease (COVID-19), caused by air droplets airborne as main transmission modes, clearly induces a spectrum clinical manifestations, but it also affects immune, gastrointestinal, hematological, nervous, renal systems. dramatic scale disorders complications arises from inadequacy current treatments absence vaccine specific anti-COVID-19 drugs to suppress viral replication, inflammation, additional pathogenic conditions. This highlights importance understanding mechanisms actions urgent need prospecting for new or alternative treatment options. objective present review is discuss challenging issue relative utility plants-derived polyphenols in fighting infections. Not only strong capacity highlighted magnifying health benefits, underlying are stressed. Finally, emphasis placed on potential ability combat via regulation its molecular targets human cellular binding well through resulting host oxidative stress, signaling pathways.

Language: Английский

Citations

66

Dipeptidyl peptidase-4 inhibition improves endothelial senescence by activating AMPK/SIRT1/Nrf2 signaling pathway DOI
Zhihui Chen, Jing Yu,

Menglu Fu

et al.

Biochemical Pharmacology, Journal Year: 2020, Volume and Issue: 177, P. 113951 - 113951

Published: April 3, 2020

Language: Английский

Citations

61

The Nrf2 Activator (DMF) and Covid-19: Is there a Possible Role? DOI
Saif Hassan, Mahmood Jasem Jawad, Salam Waheed Ahjel

et al.

Medical Archives, Journal Year: 2020, Volume and Issue: 74(2), P. 134 - 134

Published: Jan. 1, 2020

COVID-19 is a new viral illness that can affect the lungs and airways with lethal consequences leading to death of patients. The ACE2 receptors were widely disturbed among body tissues such as lung, kidney, small intestine, heart, others in different percent considered target for nCOVID-19 virus. S-protein virus was binding caused downregulation endogenous anti-viral mediators, upregulation NF-κB pathway, ROS pro-apoptotic protein. Nrf2 transcription factor that's play role generation anti-oxidant enzymes.

Language: Английский

Citations

55

Management of epigenomic networks entailed in coronavirus infections and COVID-19 DOI Creative Commons
Ranim El Baba, Georges Herbein

Clinical Epigenetics, Journal Year: 2020, Volume and Issue: 12(1)

Published: Aug. 5, 2020

Abstract Coronaviruses (CoVs) are highly diverse single-stranded RNA viruses owing to their susceptibility numerous genomic mutations and recombination. Such involve human animal pathogens including the etiologic agents of acute respiratory tract illnesses: severe syndrome coronavirus (SARS-CoV), Middle East (MERS-CoV), morbific SARS-CoV-2. Coronavirus disease 2019 (COVID-19), an emerging with a quick rise in infected cases deaths, was recently identified causing worldwide pandemic. COVID-19 outcomes were found increase elderly patients compromised immune system. Evidences indicated that main culprit behind deaths is cytokine storm, which illustrated by uncontrolled over-production soluble markers inflammation. The regulation process pathogenesis through molecular mechanism comprise virus-host interactions linked viral entry, replication transcription, escape, system control. Recognizing infections epigenetics lens will lead potential alteration gene expression thus limiting infections. Focusing on epigenetic therapies reaching clinical trials, clinically approved epigenetic-targeted agents, combination therapy antivirals drugs currently considered effective valuable approach for inflammatory overdrive

Language: Английский

Citations

55

Mitoquinone Protects Podocytes from Angiotensin II‐Induced Mitochondrial Dysfunction and Injury via the Keap1‐Nrf2 Signaling Pathway DOI Creative Commons
Zijing Zhu, Wei Liang, Zhaowei Chen

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2021, Volume and Issue: 2021(1)

Published: Jan. 1, 2021

Podocyte mitochondrial dysfunction plays a critical role in the pathogenesis of chronic kidney disease (CKD). Previous studies demonstrated that excessive fission could lead to overproduction reactive oxygen species (ROS) and promote podocyte apoptosis. Therefore, maintenance stable function is newly identified way protect podocytes prevent progression CKD. As mitochondria‐targeted antioxidant, mitoquinone (MitoQ) has been proven be promising agent for prevention injury cardiovascular Parkinson’s disease. The present study examined effects MitoQ on angiotensin II‐ (Ang II‐) induced both vivo vitro . mitochondria Ang II‐infused mice exhibited morphological functional alterations. observed fragmentation ROS production were alleviated with treatment. In , alterations morphology II‐stimulated podocytes, including membrane potential reduction, overproduction, adenosine triphosphate (ATP) deficiency, significantly reversed by MitoQ. Moreover, rescued expression translocation Nrf2 (nuclear factor E2‐related 2) decreased Keap1 (Kelch‐like ECH‐associated protein 1) podocytes. knockdown partially blocked protective II‐induced oxidative stress These results demonstrate exerts effect via Keap1‐Nrf2 signaling pathway.

Language: Английский

Citations

45

Metformin suppresses vascular smooth muscle cell senescence by promoting autophagic flux DOI Creative Commons
Shi Tai, Jiaxing Sun, Yuying Zhou

et al.

Journal of Advanced Research, Journal Year: 2021, Volume and Issue: 41, P. 205 - 218

Published: Dec. 22, 2021

Vascular smooth muscle cell (VSMC) senescence in the vasculature results vascular aging as well age-related diseases, while metformin improves inflamm-aging profile by enhancing autophagy. However, metformin's impact on VSMC is largely undefined. To test hypothesis that exerts an anti-senescence role restoring autophagic activity VSMCs and tissues. Animal models established angiotensin II (Ang II) induction physiological senescent primary from aortas of elderly patients were treated with metformin. Cellular assessed measuring amounts senescence-associated β-galactosidase markers, including p21 p53. Autophagy levels autophagy-related protein expression, transmission electron microscope, autolysosome staining. In order to explore underlying mechanism effects metformin, 4D label-free quantitative proteomics bioinformatic analyses conducted, subsequent experiments validating these findings. Ang II-dependent was suppressed Metformin also significantly improved arterial stiffness alleviated structural changes aged arteries, reduced secretory phenotype (SASP), proliferation migration VSMCs. Mechanistically, proteomic analysis indicated autophagy might contribute effects. Reduced flux observed II-induced cellular senescence; this reduction reversed Specifically, enhanced at autophagosome-lysosome fusion level, whereas blockade inhibited prevents promoting formation.

Language: Английский

Citations

41

Novel Insights into the Roles and Mechanisms of GLP-1 Receptor Agonists against Aging-Related Diseases DOI Creative Commons
Wei Peng, Rui Zhou,

Zefang Sun

et al.

Aging and Disease, Journal Year: 2022, Volume and Issue: 13(2), P. 468 - 468

Published: Jan. 1, 2022

Aging and aging-related diseases have emerged as increasingly severe health social problems. Therefore, it is imperative to discover novel effective therapeutics delay the aging process manage diseases. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), one of classes antihyperglycemic drugs, been recommended type 2 diabetes mellitus (T2DM). Moreover, GLP-1 RAs shown protect against oxidative stress, cellular senescence chronic inflammation, which are widely accepted major risk factors aging. However, their significance in or has not elucidated. Herein, we explain underlying mechanisms protective roles from a molecular, phenotypic perspective. We provide insights into broad prospect preventing treating Additionally, highlight gaps for further studies clinical applications This review forms basis on relationship between RAs.

Language: Английский

Citations

30