Aging-US

Aging-US recently published "Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics" which reported that ineffective results of clinical trials of over 200 anti-Alzheimer's drug candidates, with a 99.6% attrition rate, suggest that the current paradigm of Alzheimer's disease may be incomplete, necessitating exploration of alternative and complementary frameworks.

Results of this analysis suggest that Alzheimer’s may not be a brain disease but a progressive system-level network disorder, which is driven by chronic network stress and dyshomeostasis.

The latter can be caused by various endogenous and exogenous factors, such as chronic inflammatory conditions, infections, vascular dysfunction, head trauma, environmental toxicity, and immune disorders.

Whether originating in the brain or on the periphery, chronic stress, toxicity, and inflammation are communicated to the central nervous system via humoral and neural routes, preferentially targeting high-centrality regulatory nodes and circuits of the nervous system, and eventually manifesting as a neurodegenerative CNS disease.

In this report, the Aging-US authors outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.

Dr. Alexei Kurakinn and Dr. Dale E. Bredesen said, "Alzheimer’s disease has become a global epidemic, rapidly advancing in the last decade to become the 5th leading cause of death globally and the 3rd leading cause of death in high-income countries."

In brief, a multimodal clinical profile of a patient is used by a human expert to generate a representative set of terms that characterize the disease configuration of the patient.

The generated set serves as a query to search research literature and databases for information blocks with highest densities of query terms. Selected and rank-ordered blocks of information are analyzed by an expert to identify a parsimonious set of concepts that interconnect cliques of search terms. The identified concepts are then used as new or additional query terms in the next iteration to identify higher level connectors, until all search terms become assimilated within a parsimoniously interconnected network.

Analysis of the generated disease network by a human expert allows for formulation of de novo hypotheses.

Although searches are non-exhaustive and hypothesis generation is inevitably biased by idiosyncratic expertise and choices of human expert, the relative worth of a generated hypothesis is measured in terms of its practical utility by testing hypothesis’ predictions empirically and/or in silico.

The implications of the proposed systemic nature of Alzheimer’s disease for treatment and prevention of cognitive decline are briefly discussed.

The Kurakinn/Bredesen Research Team concluded in their Aging-US Research Paper that the promising results of an integrative, systemic, precision medicine approach to treating Alzheimer’s disease suggests that evaluating and addressing the individual organism as a whole rather than focusing exclusively on an apparently failing part may represent a promising strategy to approach other complex chronic multifactorial disorders, which warrants further exploration and development.

Full Text - https://doi.org/10.18632/aging.103883

Correspondence to: Alexei Kurakin email: [email protected] and Dale E. Bredesen email: [email protected]

Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology

Aging-US published a Special Collection on Eye Disease which included "Loss of NAMPT in aging retinal pigment epithelium reduces NAD+ availability and promotes cellular senescence" which reported that retinal pigment epithelium performs numerous functions critical to retinal health and visual function.

Here, the authors evaluated the temporal expression of key nicotinamide adenine dinucleotide -biosynthetic genes and associated levels of NAD+, a principal regulator of energy metabolism and cellular fate, in mouse RPE.

They simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability. This was confirmed in vivo in the RPE of mice injected sub-retinally with FK866 in the presence or absence of nicotinamide mononucleotide.

Dr. Pamela M. Martin and Dr. Ravirajsinh N. Jadeja said, "The retinal pigment epithelium (RPE) performs numerous functions essential to normal retinal health and function."

RPE serves as a physiologic barrier between the photoreceptor cells and the choroidal blood supply and in doing so, plays an essential role in protecting the retina from systemic insults by regulating immune responses and thereby limiting the entry of infectious or otherwise detrimental agents into retina.

This is the premise of a number of recent studies including the present investigation in which we focused on nicotinamide adenine dinucleotide and factors governing its bioavailability in relation to the overall impact on RPE viability. NAD+, a central metabolic cofactor, plays a critical role in regulating cellular metabolism and energy homeostasis. The ratio of NAD+ to NADH regulates the activity of various enzymes essential to metabolic pathways including glycolysis, the Kreb’s cycle, and fatty acid oxidation.

There is a wealth of clinical and experimental data stemming from studies of other primary diseases of aging demonstrating clearly a generalized decline in the availability of NAD+ in association with increased age and the related reduction in the activity of a number of downstream metabolic pathways that contribute to the development and progression of degenerative processes.

Members of the sirtuin family, poly ADP-ribose polymerases and the efficacy of therapies capable of impacting them have been evaluated in the context of aging retina and RPE. However, little attention has been given to upstream factors that regulate NAD+ biosynthesis, particularly in RPE. Given the importance of RPE to retinal health and function, in the present investigation we focused on evaluating the impact of NAD+ and factors that regulate its availability on RPE viability both in vivo and in vitro.

This finding is highly relevant to the clinical management of AMD but perhaps also broadly to the management of other degenerative retinal diseases in which RPE is prominently affected.

The Martin/Jadeja Research Team concluded in their Aging-US Research Output that these present data demonstrating an age-dependent decline in NAMPT expression and in turn, NAD+ generation in RPE which ultimately promotes RPE senescence supports strongly the rationale for enhancing NAMPT expression and associated NAD+ generation therapeutically.

Based upon the present experimental observations, future preclinical studies evaluating NMN or other therapies that have a direct impact on NAMPT expression and NAD+ metabolism in the context of aging and age-related retinal disease development and progression are highly warranted.

Full Text - https://www.aging-us.com/article/101469/text

Correspondence to: Pamela M. Martin email: [email protected] and Ravirajsinh N. Jadeja email: [email protected]

Keywords: retinal pigment epithelium (RPE), aging, age-related macular degeneration, NAD+, NAMPT, senescence, SIRT1

The immune system is a vast and intricate network. Seven percent of the entire human genome is composed of immune-specific genes. This complex system has important functional and maintenance roles that involve clearing out foreign pathogens and sweeping away dead or dysfunctional cells. As do most human systems, the immune system experiences degradation with age. This degradation in aging populations results in inadequate immune responses to invading pathogens, self-antigens, undesirable and malfunctioning cells, and even to vaccines.

“Furthermore, the aged immune system elicits an inadequate response to vaccines, leaving the elderly susceptible to pathogens despite being vaccinated against them. This is especially poignant in the wake of an ongoing pandemic where the mortality rate is disproportionately high in the elderly.”

Researchers from the University of Florida authored a well-written review article (with exceptionally vivid figures and illustrations) exploring a potential cause of the aging immune system. They believe therapies that could target this cause may stave off age-related diseases and improve our quality of life as we age. The paper was published by Aging (Aging-US) in 2021, and entitled, “Cellular senescence in lymphoid organs and immunosenescence.”

Full blog - https://www.impactjournals.com/journals/blog/aging/%e2%80%8b%e2%80%8bimmunosenescence-and-the-aging-immune-system/

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DOI - https://doi.org/10.18632/aging.203405

Full text - https://www.aging-us.com/article/203405/text

Correspondence to: Daohong Zhou email: [email protected]

Keywords: cellular senescence, immunosenescence, immune senescence, senescence associated secretory phenotype (SASP), thymus

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

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At present (September 2021), the direct targets of COVID-19 have been evidently clear. COVID-19 is causing the greatest threat to those of advanced age and with comorbidities. Despite this fact, there may be additional information gleaned from the accumulating stacks of clinical COVID-19 cases being aggregated around the world. A closer look at this data in sum may help researchers learn new insights about this fast spreading and quickly mutating virus. Moreover, learning about COVID-19 and its patterns may help scientists formulate better treatments and more effective vaccines.

Researchers—from Buckingham Browne and Nichols School, Brigham and Women’s Hospital, Harvard Medical School, and Biotein—conducted a new study in an effort to decipher clinical COVID-19 data from multiple countries. Their aim was to learn additional information about the impact of COVID-19 across all age distributions, including childhood. The team wrote a trending research paper that was published by Aging (Aging-US) in August 2021, and entitled, “COVID-19 mortality rate in children is U-shaped.”

Of note, one of the four authors of this research paper is the first author (and prolific teenager) named Nina Khera. This young woman (merely 15 years old) is a student and longevity researcher that is interested in preventing age-related diseases, including those related to brain aging and COVID-19. Khera is also the co-founder of a Canadian biotech company called Biotein.

Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-data-shows-unique-covid-19-patterns-in-childhood/

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DOI - https://doi.org/10.18632/aging.203442

Full text - https://www.aging-us.com/article/203442/text

Correspondence to: Vadim N. Gladyshev email: [email protected]

Keywords: mortality, COVID-19, SARS-CoV-2, pediatrics, aging

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

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In 2016, researchers—from the University of California, Buck Institute for Research on Aging, Pacific Medical Center, and Brainreader—followed up on the anecdotal results from the 10 patients in this study. They provided objective results from quantitative magnetic resonance imaging (MRI) and neuropsychological testing. The researchers authored another paper on results of the MEND protocol, which was published by Aging and entitled, “Reversal of cognitive decline in Alzheimer’s disease.” To date, this paper has generated an Altmetric Attention score of 263.

“In each of these cases, obvious subjective improvement, noted by the patient, his/her significant other, and his/her co-workers, was accompanied by clear, quantitated, objective improvement.”

The MEND protocol, also known as the Bredesen Protocol (named after the creator of the protocol, Dr. Dale Bredesen), consists of a multifaceted, tailored approach to treating each AD patient for their individual symptoms of cognitive decline—and not only a few symptoms. This strategy uses a combination of diet, lifestyle, and therapeutic interventions. Treatment is based on the hypothesis that AD occurs due to an imbalance in an extensive plasticity network in the brain. The authors note that the MEND protocol is an iterative process and designed to improve with continued patient visits.

“The therapeutic system described in this report derives from basic studies of the role of APP signaling and proteolysis in plasticity, and the imbalance in this receptor proteolysis that reproducibly occurs in Alzheimer’s disease.”

Upon clinical assessment and lab testing, patient physical and cognitive health was evaluated. Based on this assessment, patients were prescribed a lengthy personalized therapeutic system. Among other objectives, the MEND protocol recommends treating diabetes; improving sleep and digestive health; reducing stress, inflammation, and blood sugar; increasing physical exercise, intellectual stimulation, antioxidants, and vitamins; and optimizing hormone balance, synthesis of acetylcholine, nerve growth factors, and mitochondrial function.

“In each of these cases, obvious subjective improvement, noted by the patient, his/her significant other, and his/her co-workers, was accompanied by clear, quantitated, objective improvement.”

Full blog - https://www.impactjournals.com/journals/blog/aging/reversing-alzheimers-disease-symptoms/

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DOI - https://doi.org/10.18632/aging.100981

Full text - https://www.aging-us.com/article/100981/text

Correspondence to: Dale E. Bredesen, MD email: [email protected]

Keywords: neurodegeneration, cognition, biomarkers, dementia, neuropsychology, imaging, Alzheimer's disease, Apolipoprotein E

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​

Facebook - https://www.facebook.com/AgingUS/​

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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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Aging-US published "Beneficial effects of dietary supplementation with green tea catechins and cocoa flavanols on aging-related regressive changes in the mouse neuromuscular system" which reported that green tea extract (GTE) and cocoa-supplemented diets significantly improved survival rate of mice. GTE increased density of VAChT and VGluT2 afferent synapses on neuromuscular junctions.

Cocoa, but not GTE, reduced aging-associated microgliosis and increased the proportion of neuroprotective microglial phenotypes.

Dr. Jordi Calderó from IRBLleida said, "Sarcopenia, the progressive loss of skeletal muscle mass and function with age, is considered the main causative factor of the physical performance decline in the elderly."

Sarcopenia, the progressive loss of skeletal muscle mass and function with age, is considered the main causative factor of the physical performance decline in the elderly. The compromised muscular function associated to sarcopenia has a negative impact on the life quality of older adults and increases the risk for disability, fall-associated injuries, morbidity, and mortality. The authors have recently reported a marked increase in the microglial and astroglial pro-inflammatory phenotypes (M1 and A1, respectively) in the spinal cord of aged mice. This may be due to the presence of anti-inflammatory and neuroprotective (M2 and A2) glial subpopulations. Caloric restriction, based on a diet low in calories, has been shown to attenuate aging sarcopenia in various species by acting at different levels of the skeletal muscle.

Caloric restriction has also been reported to ameliorate age-related changes in rodent NMJs and to prevent MN and motor axon degeneration found to occur with aging [11, 21]. In a similar way, some dietary supplements have been shown to counteract age related changes that contribute to neuromuscular dysfunction (reviewed by [12) Plant flavonoids have gained particular attention as dietary compounds for keeping good health and preventing a number of diseases, particularly cardiac disorders and cancer.

The Calderó Research Team concluded in their Aging-US Research Output that, green tea and cocoa flavonoids from GTE and cocoa significantly increased survival rate of aged mice. Both diets preserved NMJ innervation and maturity, delayed the senescence process of the skeletal muscle, and enhanced its regenerative capacity. Future research is needed to investigate whether higher doses of flavonoid are needed and/or longer-term interventions can help restore proper motor function.

DOI - https://doi.org/10.18632/aging.203336

Full Text - https://www.aging-us.com/article/203336/text

Correspondence to: Jordi Calderó email: [email protected]

Keywords: sarcopenia, green tea, neuromuscular system, neural stem cells, aging, cocoa

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls

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Aging-US published "A model of the aged lung epithelium in idiopathic pulmonary fibrosis" which reported that Iiopathic pulmonary fibrosis (IPF) is an age-related disorder that carries a universally poor prognosis. By exposing mouse alveolar epithelial cells to repeated, low doses of bleomycin, instead of usual one-time exposures, the authors uncovered changes strikingly similar to those in the IPF lung epithelium.

They propose that this simple yet powerful tool could help uncover new biological mechanisms and assist in developing new pharmacological tools to treat the disease.

Dr. Ross Summer from The Jane and Leonard Korman Respiratory Institute as well as Dr. Freddy Romero from The Baylor College of Medicine said, "Idiopathic pulmonary fibrosis (IPF) represents one of the most aggressive and irreversible lung diseases, has an unknown etiology, and limited therapeutic options."

IPF arises from low-grade insults to the alveolar epithelium, which exhaust stem cell capacity and activate pathways that result in progressive tissue remodeling. Age represents the most significant risk factor for the development of IPF. Senescent cells are believed to drive immune cell and fibroblast activation via their production of secretory proteins (SASP), such as IL-6, TNF-β and TGF-β. Emerging evidence indicates that experimentally-induced pulmonary fibrosis can be ameliorated by targeting senescent cells for destruction [15]. This suggests a role for senolytic therapies in the treatment of IPf.

The Summer/Romero Research Team concluded in their Aging-US Research Output, "we describe a novel model of the IPF lung epithelium that displays many characteristics of the dysfunctional IPF alveolar epithelium. Given its low cost and ease of implementation, we believe our model is ideally suited for uncovering the molecular underpinnings driving mitochondrial dysfunction, cellular senescence and loss of proteostasis in IPF. Further, we believe our model is also ideally suited for high throughput testing of novel pharmacological compounds directed at the alveolar epithelium. This includes drugs aimed at eliminating dysfunction epithelial cells, such as senolytic medications and agents that aim to restore health to the IPF alveolar epithelium"

DOI - https://doi.org/10.18632/aging.203291

Full Text - https://www.aging-us.com/article/203291/text

Correspondence to: Ross Summer email: [email protected] and Freddy Romero email: [email protected]

Keywords: aging, IPF, mitochondria, proteostasis, epithelial cells

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls

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BUFFALO, NY-August 20, 2021 – Aging is indexed by Web of Science: Science Citation Index Expanded (abbreviated as Aging‑US). In June 2021, Web of Science (Clarivate Analytics) released their 2020 JCR Impact Factor. Aging is pleased to report that our 2020 impact factor is 5.682. This number has increased from last year’s 4.831. Without self-citation, Aging’s 2020 impact factor is 5.279.

Aging is listed in the Web of Science: Science Citation Index Expanded in two categories: Cell Biology and Geriatrics & Gerontology. According to the Journal Citation Indicator (JCI), Aging is ranked in the Q1 quartile in both categories.

Since 2009, Aging has published research papers in all fields of aging research including, but not limited to, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan.

This journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, and prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

To learn more about Aging, publication standards, and past or current issues, visit www.aging-us.com.

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About Impact Journals:

Impact Journals is an open-access publisher of research journals in biomedical sciences. Our publications focus on topics surrounding cancer research and all fields of aging research. Our mission is to provide scientists with the opportunity to share their exceptional discoveries, offer services that enable rapid dissemination of results, and to present vital findings from the many fields of biomedical science.

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Researchers from Virginia Commonwealth University, Translational Genomics Research Institute, and the Banner Alzheimer’s Institute took part in a research study experimenting with combinations of therapeutic agents which they believe may improve neurodegenerative disorders. In 2021, their paper was published in Aging’s Volume 13, Issue 13, and entitled, “Inhibition of heat shock proteins increases autophagosome formation, and reduces the expression of APP, Tau, SOD1 G93A and TDP-43.”

“In this paper we examined using isogenic colon cancer cells [with] several existing drugs that function by increasing autophagy and degrading misfolded proteins.”

“Aberrant expression of chaperone proteins is found in many human pathologies including cancer, in virology and in AD, ALS and HC.”

In this study, researchers tested drugs that have been used preclinically and clinically in several anticancer studies. The drugs used were: AR12, an antiviral chaperone ATPase inhibitor; Neratinib, a tyrosine kinase inhibitor; a combination of AR12 and Neratinib; Fingolimod, an immunosuppressive sphingosine l-phosphate receptor modulator; MMF, monomethyl fumarate; and a combination of Fingolimod and MMF.

The cells they tested these drug combinations on in vitro included Vero cells (African Green Monkey kidney cells), isogenic HCT116 colon cancer cells (genetically manipulated colon cancer cells), and GBM6 cells (glioblastoma cancer stem cells). They also used plasmids, antibodies, and siRNAs. Researchers acknowledged that the use of non-neuronal cells may be a limitation of this study.

“Our present studies were performed in non-neuronal cells and as a caveat, it is possible that our data in HCT116 and Vero cells will not be reflective of the same processes in neuronal cells.”

Despite this caveat, results from their research were promising. Some combinations of these drugs were capable of knocking down many disease specific proteins that form toxic aggregates inside cells and in extracellular environments via autophagy.

Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-new-drug-combinations-inhibit-stress-proteins/

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DOI - https://doi.org/10.18632/aging.203297

Full text - https://www.aging-us.com/article/203297/text

Correspondence to: Paul Dent email: [email protected]

Keywords: Alzheimer's, chaperone, GRP78, autophagy, neratinib

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

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Aging-US published "MiR-513b-5p represses autophagy during the malignant progression of hepatocellular carcinoma by targeting PIK3R3" which reported MiR-513b-5p repressed liver cancer cell proliferation, migration/invasion, and induced apoptosis in vitro.

Crucially, miR-513b-5p attenuated tumor growth of liver cancer cells in vivo.

In the mechanical investigation, the authors identified that PIK3R3 mRNA 3′UTR was targeted by miR-513b-5p and miR-513b-5p suppressed PIK3R3 expression.

PIK3R3 overexpression partly reversed miR-513b-5p-mediated autophagy, proliferation, and apoptosis of liver cancer cells.

Consequently, they concluded in their Aging-US Research Output that miR-513b-5p repressed autophagy during the malignant progression of HCC by targeting PIK3R3. MiR-513b-5p may be applied as a therapeutic target for HCC.

Dr. Rongjun Nie from The Guangxi Medical University said, "Liver cancer is a prevalent malignancy and the principal reason for tumor mortality globally, in which hepatocellular carcinoma (HCC) depicts 70–85% of the entire liver carcinoma weight."

As the previous studies, autophagy is a crucial process during liver cancer development and a potential therapeutic target for liver cancer therapy, but the mechanisms are poorly understood.

PIK3R3 acts as an oncogene of various cancers, containing glioma, lung cancer, and gastric cancer.

As several miRNAs are involved in the modulation of autophagy in HCC and based on the crucial role of miR-513b-5p in cancer development, the authors selected miR-513b-5p as an example to evaluate its function in autophagy during liver cancer progression.

In the present study, they were interested in the miR-513b-5p function in the modulation of autophagy during liver cancer progression.

They demonstrated that miR-513b-5p attenuated autophagy during the malignant progression of liver cancer by targeting PIK3R3.

The Nie Research Team concluded in their study, "miR-513b-5p repressed autophagy during the malignant progression of HCC by targeting PIK3R3. MiR-513b-5p may be applied as a therapeutic target for HCC."

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DOI - https://doi.org/10.18632/aging.203135

Full Text - https://www.aging-us.com/article/203135/text

Correspondence to: Rongjun Nie email: [email protected]

Keywords: hepatocellular carcinoma, autophagy, progression, miR-513b-5p, PIK3R3

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls

Media Contact

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