Daf-16-Dependent Longevity (WT but not daf-16 lifespan increased) 3

Dietary Restriction Response (WT but not eat-2 lifespan increased) 2

Dietary Restriction Response (WT but not eat-2 lifespan increased) 1

Daf-16-Dependent Longevity (WT but not daf-16 lifespan increased) 2

Daf-16-Dependent Longevity (WT but not daf-16 lifespan increased) 1

The life span of dauer-staged animals is either longer or shorter than that observed in control dauer animals.

The life span of dauer-staged animals is shorter than that observed in control dauer animals.

The life span of dauer-staged animals is longer than that observed in control dauer animals.

Age-linked tissue dysfunction is associated with mitochondrial degeneration manifested as organelle fragmentation and respiratory dysfunction. Efforts to mitigate downstream consequences of mitochondrial degeneration, as with ROS scavengers, have not...

Vascular endothelial cell (VEC) senescence drives organismal aging and age-related pathologies, yet the intrinsic factors preserving endothelial youthfulness remain poorly defined. Here, we identify MTR4, an evolutionarily conserved RNA helicase and ...

Aging is closely associated with dysregulation of lipid metabolism, making the modulation of lipid metabolism a promising strategy for promoting healthspan. Streptococcus thermophilus, a widely utilized probiotic, has shown potential in regulati...

Oxidative stress, as the core pathological mechanism of imbalance in the body's oxidation-antioxidation system, is a key inducer of accelerated aging and degenerative diseases. This study, based on the synergistic principle of microwave energy and fr...

Protein misfolding, aggregation, and oxidative stress contribute to aging and numerous neurodegenerative diseases, including Alzheimer's disease. Although the αA-crystallin-derived mini-chaperone peptide suppresses protein aggregation, its ther...

Lysosomal decline and proteostasis collapse are defining features of aging and major contributors to neurodegenerative vulnerability, yet interventions that preserve neuronal lysosomal function across aging remain poorly defined. Here, we identify 20...

Arsenic is a naturally occurring metalloid, and its pollution poses a global threat to humanity. Studies have shown that arsenic exposure accelerates aging, but the effects and mechanisms of sodium arsenite exposure on aging across both parental and ...

Aging is driven by multiple factors such as mitochondrial dysfunction and oxidative stress, leading to various age-related diseases. Phosphodiesterase-4 (PDE4) is a subfamily of phosphodiesterases and specifically hydrolyzes cAMP. PDE4 inhibitors hav...

Aging drives molecular changes that impair cellular and tissue function. Lipids are central to membrane structure, signaling and energy storage, yet their remodeling during aging remains unclear. Here, using cross-species, multi-tissue lipidomics, we...

Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, drives aging and age related functional decline. Natural polysaccharides from medicinal plants are promising interventions against oxi...

The adverse outcome pathways revealed that BDCPP disrupted germline stem cells (GSCs) apoptosis, transmitting reproductive signals through the kri-1-daf-16-lipl-4 signaling cascade, impairing TG hydrolysis and lifespan, while TDCPP acted through a GSC-independent route.

In Caenorhabditis elegans, 40 insulin-like peptides (ILPs) interact with DAF-2, the sole insulin/IGF receptor, to regulate lifespan and stress responses via the FOXO transcription factor DAF-16.

However, lifespan extension by Lys-Leu MRPs was not observed in sod-3 and daf-16 mutants.

These findings establish FAHD-1 and PYC-1 as antagonistic mitochondrial enzymes whose balance governs locomotion, reproduction, and lifespan in C. elegans, providing a conceptual framework for conserved links between mitochondrial metabolism and aging.

Under normoxia (O2= 21%), SKN-1 extended the lifespan of C. elegans and its stability was regulated by WDR-23.

Hypoxia has been shown to extend lifespan in Caenorhabditis elegans through mechanisms involving HIF-1 and DAF-16, but the interplay with SKN-1/Nrf, a key regulator of oxidative stress responses, remains complex.

In C. elegans, GGT reduced lipid and glucose accumulation, prolonged lifespan, and modulated the expression of insulin signaling-related genes, including daf-16 and daf-2.

Mutant worms in IIS (daf-2, daf-16, and sod-3) or autophagy-related genes (unc-51, atg-3, and atg-13) abolished the lifespan reduction.

In the nematode Caenorhabditis elegans, DAF-2 regulates dauer diapause, animal growth, and lifespan extension in a DAF-16/FOXO-dependent manner.

PAR-1 knockdown, or DAF-16 S249A, prolong lifespan, whereas phosphomimetic DAF-16 S249D suppresses the longevity of daf-2 mutants.