Endothelial SIRT-1 has a critical role in the maintenance of capillarization in brown adipose tissue

Furuuchi, Ryo; Shimizu, Ippei; Yoshida, Yohko; Katsuumi, Goro; Suda, Masayoshi; Kubota, Yoshiaki; Walsh, Kenneth; Minamino, Tohru

doi:10.1016/j.isci.2022.105424

Cited by 4 publications

(2 citation statements)

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“…The monocyte chemotactic protein-1 and transforming growth factor-ß signaling pathways are additional players in VSMC senescence [122]. There are proteins that may delay cel-lular senescence, such as sirtuins [123]. In mice, sirtuin protein 6 (SIRT6) may counteract onset of senescence in VSMCs.…”

Section: Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Senescent Cells: A Therapeutic Target in Cardiovascular Diseases

Suda

Paul

Minamino

et al. 2023

Cells

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Senescent cell accumulation has been observed in age-associated diseases including cardiovascular diseases. Senescent cells lack proliferative capacity and secrete senescence-associated secretory phenotype (SASP) factors that may cause or worsen many cardiovascular diseases. Therapies targeting senescent cells, especially senolytic drugs that selectively induce senescent cell removal, have been shown to delay, prevent, alleviate, or treat multiple age-associated diseases in preclinical models. Some senolytic clinical trials have already been completed or are underway for a number of diseases and geriatric syndromes. Understanding how cellular senescence affects the various cell types in the cardiovascular system, such as endothelial cells, vascular smooth muscle cells, fibroblasts, immune cells, progenitor cells, and cardiomyocytes, is important to facilitate translation of senotherapeutics into clinical interventions. This review highlights: (1) the characteristics of senescent cells and their involvement in cardiovascular diseases, focusing on the aforementioned cardiovascular cell types, (2) evidence about senolytic drugs and other senotherapeutics, and (3) the future path and clinical potential of senotherapeutics for cardiovascular diseases.

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Section: Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Senescent Cells: A Therapeutic Target in Cardiovascular Diseases

Suda

Paul

Minamino

et al. 2023

Cells

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“…In BAT, a high-calorie diet induces apoptosis in endothelial cells, and polyphenol suppressed this via a SIRT-1 dependent pathway, contributing to the maintenance of the capillary network and thermogenic response in BAT. 34 Low body temperature predicts poor prognosis in patients with heart failure, but the underlying mechanisms and pathologic implications are still largely unknown. My group found that BAT dysfunction developed in a murine thoracic aortic constriction heart failure model and had a causal role in promoting pathologies in the failing heart.…”

Section: Pathogenic Role Of P53 Signaling In Cardiovascular-metabolic...mentioning

confidence: 99%

Exploration of New Therapies for Heart Failure Targeting Age-Related Mechanisms

Shimizu

2024

Circ J

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Evidence indicates a role of cellular senescence and systemic insulin resistance (hyperinsulinemia) in the pathogenesis of agerelated cardiovascular-metabolic disorders, including heart failure, atherosclerotic diseases, obesity, and diabetes. "Metabolic remodeling" is one of the keywords for aging research, and studies with brown adipose tissue have shown that maintaining the homeostasis of this organ is crucial to suppressing the progression of pathologies in obesity and heart failure. The mechanisms contributing to the synchronization of aging (sync-aging) are mysterious and interesting. "Senometabolite" or "senoprotein" are defined as circulating molecules that have causal roles in sync-aging, which requires the establishment of new concepts: age-related fibrotic disorders (A-FiDs), and senometabolite-related disorders (SRDs). Globally, researchers are active in comprehensive and conclusive studies targeting age-related circulating molecules. Recently, the senolytic approach opened a new avenue for aging research. Senolysis, mediated through a genetic/pharmacologic/vaccination approach, reversed aging and pathologies in age-related diseases. Suppression of prosenescent molecules (senocules) and senolysis, the specific depletion of senescent cells, will become next-generation therapies for cardiovascular diseases.

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