A hierarchy of causes of death in senescent C. elegans.

Interventions that extend lifespan in animal models could, in principle, decelerate the aging process as a whole. Alternatively, they could act by suppressing one or more individual late-life pathologies that contribute to mortality. Here we …

43 Early
Design 5
Sample 7
Peer Review 15
Replication 6
Transparency 10

Bisdemethoxycurcumin extends lifespan and healthspan in Caenorhabditis elegans via modulation of EGFR-linked signaling pathways.

Bisdemethoxycurcumin (BDMC) is a natural curcuminoid with higher solubility and stability than curcumin, yet its potential role in lifespan and healthspan regulation remains largely unexplored. This study aimed to investigate the effects of BDMC on …

38 Early
Design 5
Sample 7
Peer Review 10
Replication 6
Transparency 10

How Lysosomes Control Aging: New Pathways to Longer, Healthier Lives

Cells have recycling centers that control aging. Better recycling may slow getting older and prevent age-related diseases.

This review examines how lysosomes—cellular recycling centers—actively regulate aging through two newly discovered signaling pathways (lysosomal surveillance response and transgenerational lysosomal signaling) and the protein TFEB. These findings suggest targeting lysosomal activity could be a …

35 Early
Design 4
Sample 2
Peer Review 13
Replication 6
Transparency 10

Senescent cells are more susceptible to reductive stress-induced cell death: implications for senolytic research.

Proliferating cells can enter an irreversible state of cell-cycle arrest known as cellular senescence. The accumulation of senescent cells contributes to organismal ageing and age-related pathologies. Consequently, therapeutic strategies have emerged to selectively eliminate senescent …

34 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 12

Hydrogel-based senomorphic approaches to modulate cellular senescence and promote tissue rejuvenation.

Cellular senescence is a major driver of age-related tissue dysfunction, characterized by chronic inflammation, oxidative stress, mitochondrial impairment, and disrupted extracellular matrix homeostasis. While senolytic strategies that eliminate senescent cells have shown therapeutic promise, irreversible …

38 Early
Design 5
Sample 7
Peer Review 10
Replication 6
Transparency 10

Manganese overload as a previously underappreciated trigger of cellular senescence: unraveling mechanisms and therapeutic rescue by the senolytic quercetin.

Manganese (Mn) is an essential trace element, but excessive Mn exposure is associated with neurotoxicity and aging-related dysfunction. Whether Mn overload promotes cellular senescence and the mechanisms involved remain insufficiently defined. Here, we investigated Mn-induced …

38 Early
Design 5
Sample 7
Peer Review 10
Replication 6
Transparency 10

Alveolar Epithelial Cell Loss of the Mitochondrial Regulator TFAM Drives Progressive Lung Fibrosis

Idiopathic pulmonary fibrosis (IPF) is characterized by failed alveolar epithelial repair and progressive fibrotic remodeling. Although aberrant reprogramming of alveolar type 2 (AT2) cells and accumulation of transitional AT2 states are increasing recognized as central …

39 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 17

How immune cells called NK cells shape healthy aging

This review synthesizes evidence that natural killer (NK) cells—a type of immune cell—undergo age-related changes that impair their ability to clear damaged cells and regulate inflammation, contributing to aging-related diseases. The authors propose NK cell …

35 Early
Design 4
Sample 2
Peer Review 11
Replication 9
Transparency 9

Lessons From Yeast: Mechanisms of Telomere Length Regulation.

Telomeres are sequences at chromosome ends that distinguish the natural end from a DNA break. Telomeres shorten at each round of cell division because the replisome cannot completely copy both DNA strands to the very …

38 Early
Design 5
Sample 7
Peer Review 10
Replication 6
Transparency 10

How aging immune systems damage lungs—and what treatments might help

If your immune system ages slower, your lungs might stay healthier longer—but we need better treatments to prove it works.

This review examines how immunosenescence (age-related immune decline) drives lung diseases like COPD, fibrosis, and cancer, and surveys emerging treatments including senolytics, stem cell therapy, and lifestyle interventions. While it synthesizes current knowledge well, it's …

36 Early
Design 4
Sample 2
Peer Review 13
Replication 7
Transparency 10

Rejuvenation Potential of Developmental Genes Downregulated in Aging.

Partial reprogramming with Yamanaka factors effectively reverses cellular aging but poses potential oncogenic risks, limiting clinical translation. To identify safer rejuvenation induction factors (RIFs), we integrated five aging datasets and compared them with single-cell transcriptomics …

46 Early
Design 5
Sample 7
Peer Review 18
Replication 6
Transparency 10

NPC1 deficiency engages a lysosome - genome - immune program linked to neurodegeneration and cellular aging signatures

Lysosomal dysfunction is a prominent feature of neurodegeneration and aging, yet how primary defects in lysosomal trafficking are converted into progressive cellular decline remains poorly understood. Niemann Pick disease type C (NPC), caused by impaired …

39 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 17

Multimodal Deep Learning Reveals the Modular Genetic Architecture of Cardiovascular Aging

Age is the dominant risk factor for cardiovascular disease, yet individuals of the same chronological age can differ markedly in the organs and biological pathways through which cardiovascular vulnerability emerges. We used deep learning to …

39 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 17

Why Aging Cells Sometimes Help—and Sometimes Hurt—Muscle Repair

Understanding how aging cells block muscle repair could lead to new treatments to help older adults stay strong and independent.

This review examines cellular senescence (aging cells that stop dividing) in muscle regeneration, finding that senescent cells play a dual role: they can briefly help repair muscle after injury, but when they accumulate in aging …

37 Early
Design 4
Sample 2
Peer Review 15
Replication 7
Transparency 9

Cutting dietary valine extends male mouse lifespan by 23%

One amino acid in protein might extend male lifespan; needs human testing to know if it matters for you.

Researchers found that lifelong restriction of valine, a branched-chain amino acid in protein, improved metabolic health and reduced aging markers in both male and female mice, but only extended lifespan in males by 23%. The …

31 Early
Design 6
Sample 10
Peer Review 3
Replication 5
Transparency 7

A Drug That Kills Aging Cells in Osteoarthritis Without Harming Healthy Ones

A candidate drug could selectively kill harmful aged cells in arthritic joints while protecting healthy ones—potentially opening a new treatment avenue.

Researchers found that mocetinostat, a drug that inhibits certain histone deacetylases, selectively kills senescent (aged) chondrocytes—cells that accumulate in arthritic joints—while leaving healthy cells intact. This discovery could lead to a new class of "senolytic" …

40 Early
Design 5
Sample 6
Peer Review 15
Replication 5
Transparency 9

Can we reverse aging by partially reprogramming cells?

This review examines 'partial reprogramming'—a technique that temporarily activates rejuvenation factors to reverse aging hallmarks in cells and tissues without turning them into cancer-prone stem cells. Early evidence suggests it can restore tissue function and …

36 Early
Design 4
Sample 2
Peer Review 13
Replication 7
Transparency 10

Targeting therapy-induced senescence across multiple breast cancer subtypes in a metastatic bone-like microenvironment

Chemotherapeutic treatment of breast cancer with Doxorubicin (DOX) can induce tumor and stromal cell senescence leading to therapy-resistance. Senescence-associated secretory phenotype (SASP) promotes secretion of pro-inflammatory and tumorigenic factors causing systemic inflammation. Combined, this can …

34 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 12

An APOC1+ inflammatory CAF-like state drives a senescent, treatment-resistant niche in rheumatoid arthritis

Objectives: Rheumatoid arthritis (RA) synovitis frequently persists despite cytokine-targeted therapies, suggesting the existence of pathogenic stromal programs that sustain chronic inflammation independently of canonical immune pathways. Although synovial fibroblasts (SF) are increasingly implicated in treatment …

34 Early
Design 5
Sample 7
Peer Review 4
Replication 6
Transparency 12

Can ginseng compounds slow aging? A review of the science and future potential

Ginseng compounds show promise against aging in lab tests, but we lack proof they work in real people yet.

This review examines ginsenosides—compounds from ginseng—and their potential anti-aging effects through mechanisms like reducing cellular stress and supporting mitochondrial health. While promising in laboratory studies, the authors emphasize that moving from bench science to functional …

35 Early
Design 4
Sample 2
Peer Review 14
Replication 6
Transparency 9