bims-minfam 2023-09-10 papers

JACC Adv. 2023 Sep;pii: 100560. [Epub ahead of print]2(7):

Life's Essential 8: Optimizing Health in Older Adults.

The population worldwide is getting older as a result of advances in public health, medicine, and technology. Older individuals are living longer with a higher prevalence of subclinical and clinical cardiovascular disease (CVD). In 2010, the American Heart Association introduced a list of key prevention targets, known as "Life's Simple 7" to increase CVD-free survival, longevity, and quality of life. In 2022, sleep health was added to expand the recommendations to "Life's Essential 8" (eat better, be more active, stop smoking, get adequate sleep, manage weight, manage cholesterol, manage blood pressure, and manage diabetes). These prevention targets are intended to apply regardless of chronologic age. During this same time, the understanding of aging biology and goals of care for older adults further enhanced the relevance of prevention across the range of functions. From a biological perspective, aging is a complex cellular process characterized by genomic instability, telomere attrition, loss of proteostasis, inflammation, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. These aging hallmarks are triggered by and enhanced by traditional CVD risk factors leading to geriatric syndromes (eg, frailty, sarcopenia, functional limitation, and cognitive impairment) which complicate efforts toward prevention. Therefore, we review Life's Essential 8 through the lens of aging biology, geroscience, and geriatric precepts to guide clinicians taking care of older adults.

Keywords: Life’s Essential 8; cardiovascular disease prevention; cardiovascular health; geriatric cardiology; geroscience

DOI: https://doi.org/10.1016/j.jacadv.2023.100560

Nat Aging. 2023 Sep 07.

Dopaminergic and noradrenergic nuclei relate to different memory types in older adults.

DOI: https://doi.org/10.1038/s43587-023-00497-9

Cell Metab. 2023 09 05. pii: S1550-4131(23)00301-7. [Epub ahead of print]35(9): 1495-1497

Metabolic elasticity: A new measure of age.

Samuel Bennett, Shogo Sato.

Promoting healthy aging is contingent on understanding the underlying mechanisms for the age-associated decline in metabolic physiology. Through developing a novel concept of "metabolic elasticity" to evaluate metabolic adaptability in response to cyclical changes in energy balance, Zhou et al. present an impactful gauge of metabolic health that is particularly relevant to aging.

DOI: https://doi.org/10.1016/j.cmet.2023.08.006

Leuk Res. 2023 Sep 04. pii: S0145-2126(23)00640-9. [Epub ahead of print] 107375

Corrigendum to "Review of clonal hematopoiesis, subtypes and its role in neoplasia and different morbidities" [Leuk. Res. 130 (2023) 1-7].

Ismail Elbaz Younes, Lee Syler, Amira Hamed.

DOI: https://doi.org/10.1016/j.leukres.2023.107375

Proc Natl Acad Sci U S A. 2023 Sep 12. 120(37): e2307449120

We need to shift the focus of aging research to aging itself.

Jesse R Poganik, Vadim N Gladyshev.

DOI: https://doi.org/10.1073/pnas.2307449120

Nat Cell Biol. 2023 Sep 04.

Depletion of p16high senescent cells for stem cell reprogramming and tissue rejuvenation.

DOI: https://doi.org/10.1038/s41556-023-01216-7

Nat Rev Immunol. 2023 Sep 04.

A platelet-derived factor protects the ageing brain.

Yvonne Bordon.

DOI: https://doi.org/10.1038/s41577-023-00939-w

BMB Rep. 2023 Sep 08. pii: 5938. [Epub ahead of print]

Fatty acid oxidation regulates cellular senescence by modulating the autophagy-SIRT1 axis.

Seungyeon Yang, Subin Moon, Soojung Claire Hur, Seung Min Jeong.

Senescence, a cellular process through which damaged or dysfunctional cells suppress their cell cycle, contributes to aging or age-related functional declines. Cell metabolism has been closely correlated with aging processes and it is widely recognized that metabolic changes underlie cellular alterations with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We find that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, the increased formation of autophagosome following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we find that the inhibition of autophagy or the enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence.