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Background/Objectives: Aging is associated with structural and functional changes in the heart, including hypertrophy, fibrosis, and impaired contractility. Cellular mechanisms such as senescence, telomere shortening, and DNA damage contribute to these processes. Nuclear factor kappa B (NF-κB) has been implicated in mediating cellular responses in aging tissues, and increased NF-κB expression has been observed in the hearts of aging rodents. Therefore, NF-κB is suspected to play an important regulatory role in the cellular and molecular processes occurring in the heart during aging. This study investigates the in vivo role of NF-κB in aging-related cardiac alterations, focusing on senescence and associated cellular events. Methods: Young and old wild-type (WT) and transgenic male mice with cardiomyocyte-specific NF-κB suppression (3M) were used to assess cardiac function, morphology, senescence markers, lipofuscin deposition, DNA damage, and apoptosis. Results: Kaplan–Meier analysis revealed reduced survival in 3M mice compared to WT. Echocardiography showed evidence of eccentric hypertrophy, and both diastolic and systolic dysfunction in 3M mice. Both aged WT and 3M mice exhibited cardiac hypertrophy, with more pronounced hypertrophic changes in cardiomyocytes from 3M mice. Additionally, cardiac fibrosis, senescence-associated β-galactosidase activity, p21 protein expression, and DNA damage (marked by phosphorylated H2A.X) were elevated in aged WT and both young and aged 3M mice. Conclusions: The suppression of NF-κB in cardiomyocytes leads to pronounced cardiac remodeling, dysfunction, and cellular damage associated with the aging process. These findings suggest that NF-κB plays a critical regulatory role in cardiac aging, influencing both cellular senescence and molecular damage pathways. This has important implications for the development of therapeutic strategies aimed at mitigating age-related cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Background: Epidemiological and toxicological studies have shown that inhalation of particulate matter (PM), a major component of air pollution, is associated with the development of cardiovascular diseases (CVDs). Cellular senescence and other aging mechanisms are also key factors in the development and progression of CVD. This study aims to investigate age-related susceptibility to cardiac remodeling and senescence due to PM exposure. Methods: Young and old male C57BL/6 mice were exposed to filtered or polluted air for six months using an ambient particle concentrator. Cardiac hypertrophy, fibrosis, and markers of cellular senescence (p53, p21, p-H2AX, and lipofuscin) in the myocardium were evaluated in the experimental groups. Results: PM exposure induces signs of cardiac remodeling, including cardiomyocyte enlargement and increased fibrosis, in young mice, along with elevated p53 expression. However, no significant alterations in cardiac structure or senescence markers were observed between aged mice exposed or not to PM. Conclusions: Our study indicates that younger individuals may be more vulnerable to the cardiovascular effects of chronic PM than older individuals exposed later. Further studies are needed to explore detailed mechanisms of this age-dependent response. [ABSTRACT FROM AUTHOR]