Reviewing the Present State of Development of Senomorphic Therapies

Vascular dysfunction in aging is driven by multiple interconnected hallmarks of aging, including DNA damage, oxidative stress, chronic inflammation, mitochondrial dysfunction, and cellular senescence and features by endothelial impairment, inflammation, and reduced nitric oxide–cyclic guanosine monophosphate (NO–cGMP) signaling.

A number of prevalent age-related conditions are notably different in timing and progression between the sexes. No doubt the list of differences by sex will grow as the research community explores the first therapies that target important mechanisms of aging.

Cerebrospinal fluid drainage from the brain into the body is necessary to remove metabolic waste from the brain.

Author Correction: Aged bone marrow macrophages drive systemic aging and age-related dysfunction via extracellular vesicle-mediated induction of paracrine senescence

Endothelial AGGF1 deficiency contributes to early vascular aging and age-elevated blood pressure via inhibiting the SESN2/p-eNOS pathway. Age-dependent AGGF1 attenuation reduces its binding to the SESN2 promoter. SESN2 downregulation induces mitochondrial respiratory dysfunction and elevated mitochondrial ROS, thereby reducing eNOS phosphorylation.

Aging Cell, Volume 25, Issue 8, August 2026.

Announcing a new article publication for Cardiovascular Innovations and Applications journal. Aging is an inevitable biological process marked by progressive functional decline and elevated risk of cardiovascular diseases (CVDs).

A review finds that restricting protein, particularly methionine, isoleucine, and valine, may improve metabolism and influence key aging pathways, largely in experimental models.

“What is true is that NMR—a single scan—can tell you a heck of a lot more than just your cardiovascular risk, your inflammation level, your diabetes risk, your mortality risk.” —Jim Otvos