LongeCityNews Last Updated: 24 April 2026 - 12:28 PM

Senescent cells accumulate with age, generating disruptive inflammatory signaling that is disruptive to tissue structure and function. Numerous research groups and companies are developing therapies capable of either selectively destroying senescent cells or dampening their signaling. Animal studies and initial human trials suggest that the earliest senolytic treatments used to clear senescent cells, derived from cancer therapies, are safe and effective enough for widespread use. The drugs and compounds used cost relatively little, which is a meaningful argument for greater exploration of their utility. Unfortunately they are not a point of focus outside academia and a small number of anti-aging physicians. Few studies have directly compared first generation senolytic treatments, so the data noted here is interesting for supporting the dasatinib and quercetin combination over navitoclax.

Genetic background is a major determinant of disc degeneration, a leading cause of chronic back pain and disability. Herein, we demonstrate that premature disc cell senescence contributes to early-onset degeneration in SM/J mice and test two systemic senotherapeutic strategies to mitigate it: Navitoclax (Nav.) and a cocktail of Dasatinib and Quercetin (DQ).

While Nav. treatment did not improve severe degeneration in SM/J mice or senescence status, DQ-treated mice showed lower grades of degeneration and a decreased abundance of senescence markers, including p19ARF, p21, and the senescence-associated secretory phenotype (SASP). DQ improved disc cell viability and phenotype retention and retarded fibrosis of the nucleus pulposus tissue. Transcriptomic analysis revealed tissue-specific effects of the treatment, with cell cycle regulation and JNK signaling being commonly affected across different tissue types. A comparison of SM/J data with DQ-mediated aging-dependent amelioration of disc degeneration in C57BL/6 N mice identified Junb and Zfp36l1 signaling as shared DQ targets in the mouse disc.

Notably, the in vitro inhibition studies of the JUN pathway in human degenerated NP cells mimicked the benefits of DQ, namely, a reduction in senescence and SASP. This study reinforces the efficacy of senolytic treatment in ameliorating local senescence and intervertebral disc fibrosis.

Link: https://doi.org/10.1038/s41413-026-00526-4

Chronic kidney disease is largely age-related, though can occur in younger people under some circumstances. It is one of a number of conditions in which research strongly implicates cellular senescence in its onset, progression, and pathology. Senescent cells accumulate in tissues with age. Cells become senescent throughout life, both on reaching the Hayflick limit to replication and in response to stress or damage. A senescent cell ceases replication, grows in size, and generates pro-inflammatory, pro-growth signaling that attracts the immune system and alters the behavior of surrounding cells. In the short term, this signaling is helpful. In youth, senescent cells are cleared efficiently by the immune system, but in later life this clearance falters allowing senescent cells to accumulate in number. Sustained senescent cell signaling contributes to chronic inflammation and disruption of tissue structure and function.

Today's open access paper reviews what is known of cellular senescence in kidney aging versus chronic kidney disease, and notes the arguments for and against considering chronic kidney disease to be a form of accelerated kidney aging. Either way, kidney disease and dysfunction is fairly high on the list of conditions that may be treated earlier rather than later in the development of senotherapeutic drugs that either selectively destroy senescent cells or modulate their behavior to be less harmful. The diabetic form of kidney disease is one of the few conditions for which an initial clinical trial using first generation senolytic drugs has taken place. The similarities between kidney aging and kidney disease might provide hope that low-cost senotherapeutics can meaningfully reduce the burden of dysfunction in older individuals.

Chronic Kidney Disease and Cellular Senescence

As individuals age, kidney function naturally declines, with the decrease in estimated glomular filtration rate (eGFR) starting at around age 30 at a rate of 0.7-0.9 mL/min/1.73 m2 per year in healthy individuals. With age, the kidney undergoes a series of changes that resemble those observed in chronic kidney disease (CKD), including a reduction in the number and size of nephrons, glomerulosclerosis, tubular atrophy, inflammation, dyslipidemia, interstitial fibrosis, and an increase in the prevalence of vascular rarefaction and arteriosclerosis. Furthermore, aging kidneys, similarly to kidneys in CKD, are susceptible to injury, oxidative stress, inflammation, and fibrosis and often struggle to regenerate and recover. However, these changes are typically milder during normal aging than in CKD. Therefore, in many ways, CKD may be likened to a state of premature or accelerated renal aging.

This resemblance partly reflects the unique physiological context of the kidney, where high metabolic activity, chronic exposure to circulating toxins, susceptibility to hypoxia, and limited regenerative capacity of key cell populations amplify stress responses and promote the accumulation of senescent cells. At the cellular level, typical features of premature aging include the accumulation of senescent cells and stem cell exhaustion. Disruption or dysregulation of critical signaling pathways, such as DNA damage, oxidative stress, telomere shortening, loss of Klotho, and oncogene activation, can lead to premature aging. Recent proteomic and transcriptomic studies provide evidence that cellular senescence contributes to CKD progression rather than solely reflecting aging.

CKD patients can be stratified into senescence-based endotypes (sendotypes), where a high-senescence signature dominated by TNF, NF-κB, and MAPK signaling is associated with worse renal function and faster eGFR decline. These senescence-associated pathways were further validated in human CKD biopsies and kidney organoid injury models, confirming their involvement at the tissue level. These findings suggest that CKD is biologically heterogeneous with respect to senescence signaling. The sendotype framework may therefore provide a basis for precision senotherapeutic strategies, where therapies targeting specific inflammatory or senescence pathways (e.g., NF-κB or MAPK signaling) could be applied to patient subgroups most likely to benefit.

The literature highlights cellular senescence as a central mechanism driving both kidney aging and CKD. Nevertheless, determining whether renal senescence serves as a catalyst or an outcome of CKD remains challenging, as current evidence suggests a bidirectional relationship in which kidney injury promotes senescence, while senescent cells further promote inflammation and fibrosis, thereby contributing to disease progression.

For those of us in the Northern Hemisphere, spring is here. This is a time of renewal and hope for better times ahead, echoing what our field is trying to achieve: the rejuvenation of aging cells and tissues to keep older people free from age-related diseases.

On that note, let’s take a look at what has been going on at Lifespan News and the wider Lifespan Research Institute.

Top longevity news stories

Kicking off the new year, we published a trio of articles covering the state of the rejuvenation research field. We engaged leading experts in business, research, and advocacy to give you an overview of how things are progressing.

Geroscience in 2025: The Expert Roundup

How far has science advanced towards longer healthier lives?

We spoke with researchers Steve Horvath, George Church, Andrea Maier, Matt Kaeberlein, and Oliver Medvedik. They shared their expert views on the current state of aging research.

Longevity Biotech in 2025: The Expert Roundup

Good science also needs good business leadership to turn discoveries into working therapies. Getting therapies through clinical trials is the final barrier to making rejuvenation biotech an accessible reality.

Kristen Fortney, Mehmood Khan, Jamie Justice, Nathan Cheng, Karl Pfleger weighed in on the business side of the field. Join us as we explore how the business of rejuvenation is progressing.

Longevity Advocacy in 2025: The Expert Roundup

Developing the technology is one thing, but that needs to be accompanied with effective advocacy. There are many misconceptions and objections to treating aging as a medical issue. We need strong advocacy to educate people and build social acceptance.

Andrew Steele, Melissa King, Bernard Siegel, Dylan Livingston, Adam Gries, and Anastasia Egorova shared their thoughts. Check out how longevity advocacy performed in 2025.

LRI was at the Longevity Biomarkers Competition

LRI President Keith Comito recently spoke at the Longevity Biomarkers Competition in Infinita City in Roatán, Honduras. The “living laboratory” event saw researchers, innovators, entrepreneurs, artists, and biohackers exploring the future of longevity science.

Keith is a technology inventor who has developed digital biomarker tools using face, body, and voice data. In his presentation, he suggested that these non-invasive “functional biomarkers” may solve a key challenge in aging research. They could provide reliable, treatment-sensitive signs of biological age for clinical trials.

Prioritizing audio/video-based biomarkers could deliver quick wins and drive broader adoption. For example, most dementia cases go undiagnosed because doctors rarely screen for it. However, voice-based technology has the potential to detect dementia early. Paired with new drugs, it may reduce progression and yield major economic benefits.

In addition to chronic conditions, this diagnostic potential also applies to infectious diseases. During the COVID-19 pandemic, Keith worked on projects surrounding vocal diagnostics of the disease using Convolutional Neural Networks (CNNs).

CNN-based vocal diagnostics can detect infectious diseases like COVID-19 by analyzing vocal cord and respiratory features. These models reportedly outperformed antigen tests versus PCR, detecting even asymptomatic cases with high specificity. They work because COVID affects the nervous system, so models can detect subtly altered vocal cord vibrations rather than relying on phlegm.

This may be useful for other conditions that affect the neurological system, such as Alzheimer’s disease. In fact, it may have broad applications for a variety of diseases that have a subtle influence on the voice.

Non-invasive functional biomarkers, if developed properly, could become a useful accompaniment to traditional medical screening. In the future, it isn’t hard to imagine something akin to the Star Trek medical tricorder using these technologies.

Rapamycin and exercise clinical trial results

We are delighted to see that Dr. Brad Stanfield has had his manuscript accepted. LRI (at the time Lifespan.io) supported Brad’s fundraising efforts to get this clinical trial launched.

Congratulations to Brad, and we are glad we were able to help. We look forward to seeing the published results of his rapamycin clinical trial.

Radical No More: Societal Perceptions of Life Extension – Past, Present, and Future Directions

Keith Comito has also recently contributed to a publication focusing on how society suffers from mixed messaging. He argued that the public does, in fact, support longer lifespans. He also proposes that our field should be less inclined to downplay the potential rewards of its success.

There should be nothing radical about the idea of living longer thanks to medical technology that targets aging. It does seem somewhat strange that the concept of more and healthier years should be somehow taboo. It makes us wonder if people in the past pushed back on other technologies that allowed people to live longer in good health. Somehow, we doubt that happened in any significant capacity.

A good example of that support would be a 2022 AARP and National Geographic collaborative survey, which included 2,580 US adults. In one part, they asked them a simple question: “Assume for a moment that there was a pill that could extend your life by 10 years. How likely would you be to take that pill?”

The response to that question was largely in favor of taking that pill and enjoying additional years of life. This seems to go against the persistent narrative that these ideas are somehow radical and unpopular.

The same survey went on to couch those additional years with continued good health. The results are even more in favor of using rejuvenation technologies to increase healthy lifespans. With the understanding that those additional years will be spent in good health, there is a significant increase in support.

Keith went on to discuss other examples of support and enthusiasm for increasing human lifespans.

Abstract

Humanity’s relationship with mortality has long defined its values, myths, and ambitions. Across cultures, the quest to transcend aging has been reflected in stories that both explore the desire for life extension and warn against its pursuit.

However, as the science of longevity advances, these inherited narratives, once serving to reconcile people with inevitable death, now distort public understanding and policy by linking life extension with moral corruption, inequality, or futility.

This tension reflects a psychological coping pattern that evolved in response to perceived impossibility, not genuine opposition to longer life itself. Analysis of mythological motifs, cultural history, social media data, and contemporary polling reveals that broad public support exists for increased healthspan and even radical lifespan gains, provided they are equitable and grounded in credible science.

These findings challenge the assumption that advocacy must downplay longevity goals for wider acceptance. Recognizing and updating these cultural scripts opens new pathways for public engagement, research funding, and ethical frameworks that align emerging biotechnologies with our enduring human aspiration, to live longer, healthier, and more meaningful lives.

Keith provided some real food for thought ,and perhaps our field needs to change how it thinks about public engagement. Check out the full Radical No More article.

Longevity Day at NFC Summit Lisbon has announced its confirmed speaker lineup ahead of its debut on 4 June 2026 at the Unicorn Factory in Lisbon. The event will bring together scientists, clinicians, founders, and investors from across the longevity ecosystem for a full-day program spanning ancestral wisdom, cutting-edge science, and frontier biotech.

The event is curated by Michelangelo Gallia and Nina Patrick, co-founders of Longevity Wednesdays in Lisbon, and is embedded within NFC Summit, one of Europe’s largest tech and entrepreneurship conferences, drawing 4,000 attendees from 59 countries.

A LINEUP ACROSS THREE THEMATIC PILLARS

Longevity Day is structured around three tracks: Wisdom from the Past, Knowledge from the Present, and Hope from the Future — a framework that holds ancestral practice and radical science with equal seriousness.

Confirmed speakers include:

• Diogo Barardo — R&D Director, NOVOS (Knowledge from the Present)
• Dr. Jeff Vogel — Physician & CEO, Concorde Health (Knowledge from the Present)
• Marvin Amberg — Consumer Health Investor, naturalX Health Ventures (Knowledge from the Present)
• Dr. Sabine Krofczik-Wilhelm — Neurodegenerative Disorders, PPD/Thermo Fisher (Knowledge from the Present)
• Francisco Marques-Teixeira — Founder & CEO, Mu Labs (Wisdom from the Past)
• Stephen Watson — Founder, Miami Institute; former CSO, Blue Zones Center (Knowledge from the Present)
• Jose Pedro Castro — Researcher & Professor, i3s & NOVA Medical School (Knowledge from the Present)
• Anthony Schwartz — CEO, ARTAN Bio (Hope from the Future)
• Max Unfried — Research Fellow, National University of Singapore; Scientific Director, The Thalion Initiative (Hope from the Future)
• Max Rodman — Founder, MVMT.Studio (Wisdom from the Past)
• Caitlin Lewis — Research Director & Founding Board Member, LEV Foundation (Hope from the Future)
• Yves Beraerts — Neuroscientist & Wim Hof Method Instructor, Champalimaud Foundation (Wisdom from the Past)
• Borjan Miliniković — Postdoctoral Researcher, Institut des Neurosciences Paris-Saclay (Hope from the Future)
• Sebastian Brunemeier — Partner & Co-Founder, Healthspan Capital & LongGame Ventures (Hope from the Future)
• Ekua Yankah — Public Health Strategist & Founder (Wisdom from the Past)

ABOUT LONGEVITY DAY AT NFC SUMMIT LISBON

Longevity Day is a dedicated track within NFC Summit, Europe’s premier technology and entrepreneurship conference. The event takes place on 4 June 2026 at the Unicorn Factory, Lisbon. It is the only longevity event in Portugal to convene researchers, founders, clinicians, and practitioners across this breadth of the field in a single day.

Tickets and registration: https://www.eventbrite.pt/e/longevity-day-2026-tickets-1984404402988

ABOUT NFC SUMMIT

NFC Summit is one of Europe’s largest technology and entrepreneurship conferences, hosting 4,000 attendees from 59 countries annually in Lisbon, Portugal.

For press inquiries, speaker interviews, or partner information, contact Michelangelo Gallia at michelangelo@frontaeva.com