Compared to the issues that come with, say, a failing liver, skin aging can look like more of a vanity problem. But aging in both tissues, and multiple others, is driven by the same underlying molecular mechanisms. One of those mechanisms is fibrosis, the cross-linking of extracellular matrix (ECM) proteins that leads to tissue stiffening. Anti-aging company Cambrian Biopharma Inc. has argued that stiffening of the ECM should be considered one of the formal hallmarks of aging.

Epigenetic testing company Trudiagnostic LLC has linked up with Rejuve.AI, an artificial intelligence (AI)-powered longevity research network, to develop more accurate tools for predicting chronological age. Specifically, the collaboration seeks to shed new light on the biology of aging and connectedness of DNA methylation (DNAm), metabolomics and proteomics.

“Short-lived organisms represent a fundamentally different evolutionary strategy, and the idiosyncrasies influencing their aging may not apply to longer-lived models, including humans,” researchers from Harvard Medical School wrote in the Jan. 11, 2023, issue of Science Advances.

In their paper, the authors reported insights into the genomics of longevity that took advantage of an unusual animal model: rockfish.

The first in vivo cell atlas of senescent tissue in skeletal muscle has identified the damaging properties of these cells and explained why they block muscle regeneration. According to a study at Pompeu Fabra University led by scientists from Altos Labs Inc., cell damage caused the senescence of the cells, which secreted toxic substances into the surrounding microenvironment, causing fibrosis and preventing tissue regeneration.

Low-dose administration of anti-PD-1 monoclonal antibodies could potentially reverse conditions associated with aging such as the accumulation of senescent cells and inflammation, according to a new study conducted at the Institute of Medical Science at the University of Tokyo.

Disrupted meiosis, the cell division process that leads to the production of reproductive cells in sexually reproducing organisms, led to a decline in overall health by triggering an accelerating aging signature in the roundworm Caenorhabditis elegans.

The work is “the first direct evidence that manipulating the health of reproductive cells leads to premature aging and a decline in healthspan,” senior author Arjumand Ghazi, an associate professor of pediatrics, developmental biology, and cell biology and physiology at the University of Pittsburgh and the University of Pittsburgh Medical Center (UPMC) Children’s Hospital, said in a press release.

Fibroblasts expressing the tumor suppressor p16INK4a (a marker of senescence) stimulated lung stem cells from young mice to repair damaged tissue, according to a study from the University of California, San Francisco (UCSF). The finding calls into question therapies that eliminate these senescent cells without considering their beneficial role in tissue homeostasis.

By independently manipulating the lifespan of worms and one of its purported biomarkers, namely, the cessation of vigorous movement (CVM), investigators at the Center for Genomic Regulation (CRG) in Barcelona have demonstrated that the two are driven by partly independent processes.

Researchers have gained new insights into both genetic and nongenetic factors affecting life span, and how they differ between males and females. Several genes were correlated with longevity, according to a study by the École Polytechnique Fédérale de Lausanne (EPFL). However, some did not affect life span until males reached a certain age. Early access to nutrients during growth also affected longevity, as they saw in their study of more than 3,000 mice and verified with human data. “This study is one of the biggest studies on mass longevity. We were looking for genetic determinants of longevity but there are non-genetic determinants affecting longevity,” the first author Maroun Bou Sleiman, researcher at EPFL, told Bioworld.