In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”

DOI - https://doi.org/10.18632/aging.206132

Corresponding Author - Julia M. Sidorova - julias@uw.edu

Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE

Abstract

Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it.

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Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Aging (Aging-US)

Longevity & Aging Series (S3, E2): Dr. Julia Sidorova

BUFFALO, NY - April 28, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on April 24, 2025, titled “PD-L1 and FOXP3 expression in high-grade squamous intraepithelial lesions of the anogenital region."

Researchers Humberto Carvalho Carneiro, Rodrigo de Andrade Natal, José Vassallo and Fernando Augusto Soares from the Instituto D’Or de Pesquisa e Ensino and Rede D’Or studied early tissue changes caused by human papillomavirus (HPV) in the anal, vulvar, and penile regions. They found that high-grade pre-cancer lesions triggered stronger immune responses and showed higher levels of two immune-related markers, PD-L1 and FOXP3. These findings are important because they help explain how some HPV-related lesions progress to cancer while others heal on their own.

High-risk HPV is known to cause several types of anogenital cancers. Before these cancers appear, the virus often leads to abnormal tissue changes known as high-grade squamous intraepithelial lesions. Many of these lesions disappear without treatment, but some become cancer—especially in people with weakened immune systems. This study explored how immune activity may play a role in this progression.

The researchers examined tissue from 157 patients—95 males and 55 females—with either high-grade or low-grade HPV-related lesions. They found that T-regulatory cells, marked by the FOXP3 protein, were more common in high-grade lesions. These immune cells are known to suppress immune responses, which can allow infected or abnormal cells to grow. The team also found higher expression of PD-L1, a protein that helps cells evade immune detection, particularly in inflammatory immune cells.

"Dense inflammatory infiltrates and high counts of FOXP3+ cells were significantly more frequent in patients with HSILs than in those with LSILsHR (p = 0.04 and 0.02, respectively). HSILs also exhibited higher PD-L1 expression (padj < 0.01 and < 0.01 for the SP142 and 22C3 clones, respectively), based on the Poisson generalized linear model.”

These findings suggest that HPV may begin avoiding the immune system early in infection, even before cancer develops. The combination of high FOXP3 and PD-L1 levels may create a protective environment for infected cells, making them harder for the body to eliminate. This immune evasion may allow the lesions to remain and, over time, become cancerous.

The study also compared patients with and without HIV to assess whether immune health influenced the results. While those with compromised immune systems had more extensive lesions, PD-L1 and FOXP3 expression was also found in patients with healthy immune systems. This evidence shows that immune evasion by HPV can happen regardless of a person’s immune status.

Understanding how PD-L1 and FOXP3 function in early HPV-related lesions may help clinicians predict which lesions are more likely to become cancer. These insights could lead to new strategies for monitoring, treating, or preventing HPV-related precancerous lesions and cancer in the anogenital region. The study highlights how early immune system changes can play a key role in the development of HPV-related cancers.

DOI - https://doi.org/10.18632/oncotarget.28715

Correspondence to - Humberto Carvalho Carneiro - humberto.carneiro@rededor.com.br

Video short - https://www.youtube.com/watch?v=6d8G8TUbgYc

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Oncotarget

Early Immune Evasion Found in HPV-Related Pre-Cancer Lesions of the Anogenital Region

In this #episode of the Longevity & Aging Series, Dr. Stephen Vatner from the Department of Cell Biology and Molecular Medicine at Rutgers New Jersey Medical School, joins host Dr. Evgeniy Galimov to discuss a #research perspective he co-authored in Volume 16, Issue 22 of Aging (Aging-US), titled “Brown adipose tissue enhances exercise performance and healthful longevity.”

DOI - https://doi.org/10.18632/aging.206179

Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu

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Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ

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Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14

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Longevity & Aging Series (S3, E3): Dr. Stephen Vatner

BUFFALO, NY — April 29, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 20, 2025, titled “Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP).”

Researchers, led by first author Sudipta Bar and corresponding authors Amit Sharma and Pankaj Kapahi from the Buck Institute for Research on Aging, have found that the enzyme ADAM19 plays an important role in regulating aging in cells and inflammation in the gut. Their study shows that blocking ADAM19 reduced gut damage and inflammation in fruit flies, mice, and human cells. This discovery points to a new possible way to treat gut disorders related to aging by reducing the harmful signals from senescent (aging) cells.

As individuals age, DNA damage can lead to the accumulation of senescent cells, contributing to tissue damage. These are cells that stop dividing and release harmful inflammatory substances called the senescence-associated secretory phenotype (SASP). In this study, researchers used fruit flies to search for genes involved in radiation-related gut damage. They identified a gene called meltrin, which is similar to human ADAM19. When meltrin was turned off, the flies had less gut leakage, less inflammation, and fewer signs of cellular aging.

“Through an unbiased genome-wide association study (GWAS) utilizing 156 strains from the Drosophila Genetic Reference Panel (DGRP), we identified meltrin (the drosophila orthologue of mammalian ADAM19) as a potential modulator of the senescence-associated secretory phenotype (SASP).”

To test if these results applied beyond flies, the team inhibited ADAM19 in mice using a drug called batimastat. Mice treated with the drug after chemotherapy exposure had stronger gut barriers and lower levels of inflammatory markers. The findings extended to human cell cultures, where ADAM19 inhibition reduced signs of cellular aging, including the expression of SASP proteins and β-galactosidase, a classic aging marker. 

Importantly, this approach does not kill aging cells like many 'senolytic' therapies but instead reduces the harmful substances they release, making it a potential "senomorphic" strategy. The study also showed that ADAM19 helps release certain SASP proteins by cutting them at the cell surface, suggesting a direct role in regulating inflammatory signals.

Through proteomic analysis, the team identified 12 SASP proteins that were significantly reduced when ADAM19 was blocked. Many of these proteins are linked to inflammation, immune response, and tissue remodeling in diseases such as inflammatory bowel disease and Crohn’s disease. This connection underlines the relevance of the findings for treating chronic gut disorders in aging populations.

By targeting ADAM19, researchers may have found a new way to protect gut health and lower inflammation caused by aging cells. This study offers a promising path for creating treatments that maintain healthy tissues without having to destroy aging cells, which could benefit people with gut damage related to aging or medical treatments.

DOI - https://doi.org/10.18632/aging.206224

Corresponding authors - Amit Sharma - amit.sharma@sens.org, and Pankaj Kapahi - pkapahi@buckinstitute.org

Video short - https://www.youtube.com/watch?v=dRfxQ20O2fQ

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Inhibiting ADAM19 Reduces Gut Inflammation and Cell Aging Markers Across Species

BUFFALO, NY — May 1, 2025 — A new #research paper was #published in Aging (Aging-US) on April 2, 2025, as the #cover of Volume 17, Issue 4, titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.”

In this study, the team led by first author Sofie Lautrup and corresponding author Evandro F. Fang, from the University of Oslo and Akershus University Hospital in Norway, discovered that cells from people with Werner syndrome (WS)—a rare genetic disorder that causes  premature aging—have low levels of a molecule called NAD+ in their mitochondria. This molecule is essential for energy production, cellular metabolism, and maintaining cell health. The researchers also found a potential way to improve cell function in WS patients, pointing to new directions for treating age-related decline and other premature aging disorders.

Werner syndrome leads to signs of aging much earlier than normal, including problems such as cataracts, hair loss, and atherosclerosis by age 20 to 30. The team found that when the WRN gene is missing or damaged, cells cannot maintain healthy NAD+ levels in their mitochondria. As a result, the cells age more quickly and stop growing properly. When the researchers boosted NAD+ levels using nicotinamide riboside (a vitamin B3 compound) the affected stem cells and skin cells from patients showed less aging and improved mitochondrial activity.

“Interestingly, only 24 h treatment with 1 mM nicotinamide riboside (NR), an NAD+ precursor, rescued multiple pathways in the WRN−/− cells, including increased expression of genes driving mitochondrial and metabolism-related pathways, as well as proliferation-related pathways.”

The study also found that the WRN gene helps regulate other important genes that control how NAD+ is made in the body. Without WRN, this system becomes unbalanced, which affects how cells function, grow, and respond to stress. Although adding more NAD+ helped some cells look healthier, it could not completely fix the growth problems in other types of lab-grown cells. This suggests that while NAD+ supplementation is beneficial, it cannot fully replace the essential functions of the WRN gene.

These findings offer new insights into the biological mechanisms of aging and reinforce the therapeutic potential of targeting NAD+ metabolism in age-related and genetic diseases. Future studies will aim to better understand how subcellular NAD+ regulation interacts with mutations like those seen in WS. Finally, this research supports ongoing efforts to develop NAD+-based treatments that could slow cellular aging and improve quality of life for patients with premature aging conditions.

DOI - https://doi.org/10.18632/aging.206236

Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no

Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU

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Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation

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Boosting NAD+ Levels Slows Aging in Cells from Werner Syndrome Patients

Aging (Aging-US) invites #submissions for a Special Collection dedicated to the theme of cellular #senescence, spanning its basic mechanisms, physiological and pathological functions, and clinical applications.

This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis. Her legacy continues to inspire generations of scientists working to decode the complex biology of senescent cells and their impact on health and disease.

We welcome original research articles, reviews, and perspectives on topics including:

-Fundamental mechanisms of senescence induction and maintenance

-Regulation and context-specific roles of the senescence-associated secretory phenotype (SASP)

-Beneficial and detrimental effects of senescent cells in vivo

-Senescence in development, aging, regeneration, and age-related diseases

-Biomarkers, imaging, and tools for senescence detection and quantification

-Therapeutic targeting of senescent cells: senolytics, senomorphics, and clinical translation

This Special Collection is guest edited by Han Li and Irina Conboy, both internationally recognized leaders in the study of senescence and aging.

Submission Details:

-Submission Deadline: January 15, 2026
-Manuscript Format: Please follow the journal’s submission guidelines
-Peer Review: All submissions will undergo a rigorous peer-review process
-Submission Link: https://aging.msubmit.net/cgi-bin/main.plex

Call for Papers: Commemorative Collection Honoring Dr. Judith Campisi

BUFFALO, NY – May 5, 2025 – Aging (Aging-US), #published by Impact Journals, is pleased to #announce its participation at the upcoming Society for Scholarly Publishing (SSP) 47th Annual Meeting. The #event will take place from May 28-30, 2025, in Baltimore, Maryland.

Attendees are invited to visit Booth No. 209 to meet members of the Aging (Aging-US) team. The 2025 meeting theme, “Reimagining the Future of Scholarly Publishing at the Intersection of Value and Values,” underscores the urgency of adapting to rapid technological change, including AI, and addressing growing concerns around research integrity and trust. These priorities align closely with our mission to foster open, reliable, and impactful scientific communication in the field of aging and age-related diseases.

In addition, the Longevity & Aging Series - hosted by Dr. Evgeniy Galimov and presented by Aging (Aging-US) - is a Finalist for a Society for Scholarly Publishing (SSP) 2025 EPIC Award in the Video/Film category. Winners will be announced at the EPIC Awards Celebration on May 29.

We look forward to connecting with SSP 2025 attendees to share more about Aging (Aging-US) and our publishing initiatives.

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Aging (Aging-US) to be Featured at SSP 47th Annual Meeting in Baltimore

BUFFALO, NY - May 5, 2025 – Oncotarget, #published by Impact Journals, is proud to #announce its presence as an #exhibitor at the 47th Annual Meeting of the Society for Scholarly Publishing (SSP), taking place May 28–30, 2025, at the Hilton Baltimore in Maryland. 

Impact Journals publishes scholarly journals in the biomedical sciences, with a focus on cancer and aging research.

Attendees are invited to stop by Booth #209 to meet members of the Oncotarget team and learn more about the journal’s latest initiatives. This year’s conference theme, “Reimagining the Future of Scholarly Publishing at the Intersection of Value and Values,” highlights critical topics such as artificial intelligence, research ethics, and transparency in science—principles that closely align with Oncotarget's commitment to rigorous peer review and scientific integrity.

We look forward to connecting with SSP attendees to discuss Oncotarget’s mission, explore potential collaborations, and emphasize the role of open science in advancing cancer research and related fields.

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Oncotarget Participation at SSP 2025 Annual Meeting

BUFFALO, NY — May 6, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 2, 2025, titled “Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.”

In this study, researchers at Johannes Kepler University Linz found that fisetin, a natural substance found in fruits and vegetables, helps protect blood vessels from hardening, which is a common problem in older adults and people with kidney disease. This discovery highlights fisetin’s potential to prevent vascular calcification and reduce cardiovascular damage caused by aging and chronic kidney disease.

The research, led by first author Mehdi Razazian and corresponding author Ioana Alesutan, focused on vascular calcification—a condition in which blood vessels stiffen due to calcium deposits. This process is common in aging and chronic kidney disease and increases the risk of heart attacks and strokes. Using human and mouse study models, the researchers tested fisetin’s ability to prevent this calcification in vascular smooth muscle cells (VSMC), which play a key role in maintaining vessel health. Fisetin, known for its anti-inflammatory and antioxidant properties, significantly reduced calcium buildup and calcification markers under stress conditions that mimic disease.

The team also discovered that fisetin suppresses activity in a signaling pathway called p38 MAPK, which is known to promote calcification. This effect depends on a protein called DUSP1. When DUSP1 was blocked, fisetin could no longer protect the cells, showing that this protein is essential for its anti-calcification activity. The researchers confirmed fisetin’s protective effects in isolated mouse arteries and in living mice treated with high doses of vitamin D, which typically increases arterial calcification.

“Mechanistically, fisetin requires the phosphatase DUSP1 to inhibit p38 MAPK in order to mediate its protective effect on VSMC calcification.”

Importantly, the researchers tested fisetin under conditions similar to human disease. When VSMCs were exposed to blood serum from kidney dialysis patients—a condition known to trigger vascular calcification—fisetin again reduced calcium buildup and protected the cells. These findings suggest fisetin could be useful in countering the harmful vascular effects seen in chronic kidney disease.

This study adds to growing evidence that fisetin may protect blood vessels from aging-related damage. While more research is needed before it can be used in clinical treatments, the study highlights fisetin as a promising candidate for slowing or preventing vascular calcification. The findings could have broad implications for aging populations and individuals with kidney disease, who are at greater risk for heart problems due to vascular stiffening.

Read the full paper: DOI: https://doi.org/10.18632/aging.206233

Corresponding author: Ioana Alesutan – ioana.alesutan@jku.at

Keywords: aging, vascular calcification, vascular smooth muscle cells, fisetin, dual-specificity phosphatase 1, p38 MAPK

______

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Fisetin, a Natural Compound, Helps Prevent Artery Hardening from Aging and Kidney Disease

BUFFALO, NY — May 7, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 4, 2025, titled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”

A research team led by first author Mauricio Moel and corresponding author Stefanie L. Morgan from AgelessRx conducted a clinical trial to determine whether low-dose, intermittent rapamycin could safely improve healthspan in older adults. The findings suggest rapamycin may offer measurable benefits for physical function and overall well-being, reinforcing its potential as a safe intervention to support healthy aging.

Aging remains the leading cause of chronic conditions such as heart disease, diabetes, and dementia. While medical advances have extended lifespan, many people still experience declining health and reduced mobility in later years. This growing gap between lifespan and healthspan has driven interest in therapies that target aging itself. Rapamycin, an FDA-approved drug originally used in transplant medicine, has drawn attention for its ability to influence aging-related pathways in animal studies. Until recently, its safety and benefits in healthy human populations were largely unknown.

The PEARL trial is the longest study so far to explore rapamycin’s use for longevity in healthy aging adults. Researchers followed 114 participants aged 50 to 85 over 48 weeks in a randomized, double-blind, placebo-controlled design. Participants received either a placebo or 5 mg or 10 mg of compounded rapamycin once per week. The study’s primary goal was to measure changes in visceral fat, while secondary outcomes included lean muscle mass, blood markers, and quality-of-life assessments.

The trial found that low-dose rapamycin was safe and well-tolerated, with serious side effects reported at similar rates across all groups. The most frequent minor issue among rapamycin users was mild gastrointestinal discomfort. While no significant reductions in visceral fat were observed, women taking 10 mg of rapamycin showed significant gains in lean muscle and reported reduced pain. In addition, participants taking 5 mg weekly reported improvements in emotional well-being and general health, as measured by validated surveys.

“Our findings provide evidence that these rapamycin regimens are well tolerated with minimal adverse effects when administered for at least one year within normative aging individuals.”

Researchers noted some limitations, including the relatively small and health-conscious participant group, which may have limited the ability to detect larger effects. The compounded form of rapamycin used also had lower absorption than commercial versions, possibly reducing its impact.

Overall, the PEARL trial provides early clinical evidence that low-dose rapamycin may help support physical and emotional well-being in older adults. Further studies with larger and more diverse populations will be essential to confirm the study results and refine dosing strategies for broader application.

DOI: https://doi.org/10.18632/aging.206235

Corresponding author: Stefanie L. Morgan – stefanie@agelessrx.com

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Keywords: rapamycin, aging, healthspan, longevity, geroscience

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Low-Dose Rapamycin Improves Muscle Mass and Well-Being in Aging Adults

A recent #study from Assiut University Hospital in Egypt, published in #Oncotarget, presents a promising strategy for patients with metastatic #colorectalcancer (mCRC). The #research introduces a gentler yet effective maintenance therapy that may extend survival, enhance quality of life, and offer a more accessible treatment option for mCRC patients worldwide.

The Challenge of Treating Metastatic Colorectal Cancer

Colorectal cancer is one of the most common causes of cancer-related deaths worldwide. When it spreads to other parts of the body—a stage known as mCRC—it becomes much more difficult to treat. At this stage, clinicians often use strong drug combinations like FOLFOX or CAPOX, which mix chemotherapy drugs to stop cancer growth. FOLFOX combines three drugs given intravenously, while CAPOX includes two of the same drugs, with one taken as a pill.

While effective, these treatments can cause serious side effects. For example, one of the main drugs, oxaliplatin, can lead to nerve damage, making it painful or difficult to use the hands and feet. Fatigue, diarrhea, and other issues are also common. Over time, these side effects may force clinicians to stop or adjust the treatment, even if it is working.

That is where maintenance therapy comes in. After the cancer is controlled, clinicians often switch to a gentler treatment plan to keep it from returning. The challenge is finding a therapy that continues to work without causing too many side effects, especially in places where access to expensive or intensive treatments is limited.

Full blog - https://www.oncotarget.org/2025/05/07/panitumumab-and-low-dose-capecitabine-a-promising-maintenance-therapy-for-metastatic-colorectal-cancer/

Paper DOI - https://doi.org/10.18632/oncotarget.28687

Correspondence to - Doaa A. Gamal - doaaalygamaal@gmail.com

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Keywords - cancer, Panitumumab, maintenance, colorectal cancer, Capecitabine

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Panitumumab & Low-Dose Capecitabine: Promising Maintenance Therapy for Metastatic Colorectal Cancer

Cancer and aging are two sides of age-related tumorigenesis.

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

Longevity & Aging Series (S3, E2): Dr. Julia Sidorova

Aging (Aging-US) Podcast

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