Anti Aging Research Paper

Aging drives the occurrence of several debilitating diseases including, cardiovascular diseases (CVDs), cancer, neurodegenerative diseases and diabetes mellitus (DM). Recent experiments indicate that young plasma rejuvenates old mice and reverses age-associated pathologies. However, the systemic anti-aging factors remain poorly identified. Here we demonstrate the role of apelin (apln) in mammalian aging and identify it as a novel anti-aging factor. We show that apln and its receptor (aplnr) undergo an age-dependent decline in multiple organs. Declining apln levels perturb organismal homeostasis, as mice harboring genetic loss of apln (apln-/-) or aplnr (aplnr-/-) exhibit an age-dependent enhancement of their cardiovascular, renal, metabolic
CVDs are the leading cause of death in the age group of 65 years and above, which comprises 15% of the US population. Further identification of pathways regulating aging is, therefore, imperative to lighten the burden of aging on global health and prolonging human healthspan. Recent reports demonstrate that young plasma successfully reverses age-associated pathologies in old mice. Evidently, an age-dependent decline of, sparsely identified, pro-youthful factors contribute to the aging process while their recovery rejuvenates and restores organ functions. However, knowledge of these pro-youth or anti-aging factor(s) remains elusive. Further identification of these factor(s) is necessary to benefit age-associated debilitating diseases therapeutically and address the lack of biomarkers detailing the rapidity of
While some in vivo studies have identified it to be a vasodilator, the physiological relevance of endogenous apln remains unclear. Multiple studies have reported lower apln in patients diagnosed with hypertension (HTN), heart failure, pulmonary fibrosis, renal failure and DM. Apln-/- mice also display an enhanced progression of neurodegenerative diseases. Hence, we hypothesize that apln is a previously undiscovered anti-aging factor, and its adequate levels are necessary for organismal homeostasis. Though some in vitro studies report that apln protects against apoptosis, its effect on cellular senescence and mammalian aging have never been documented. Additionally, there is limited understanding of if and how apln levels vary with age and whether manipulating its level affects the onset and progression of