Remodeling of the intercalated disc related to aging in the mouse heart

Bonda, Tomasz A.; Szynaka, B; Sokołowska, Magdalena; Dziemidowicz, Magdalena; Winnicka, Maria M.; Chyczewski, L; Kamiński, Karol

doi:10.1016/j.jjcc.2015.10.001

Cited by 45 publications

(33 citation statements)

References 42 publications

(42 reference statements)

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“…Thus, higher amounts of lipofuscin are representative of accelerated aging and/or alterations in lipid metabolism. Studies in mice indicate that aging or senescence normally decreases Cx43 expression and function in the heart, 65 a condition different from the increase observed in our study. Furthermore, studies using SIV-infected monkeys indicate a critical role of CCR5 in gp120-mediated inflammation, recruitment of monocytes/macrophages into the cardiac tissue, and compromise of cardiac muscle and function.…”

Section: Discussioncontrasting

confidence: 99%

HIV-Associated Cardiovascular Disease

Prevedel

Morocho

Bennett

et al. 2017

The American Journal of Pathology

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Chronic HIV infection due to effective antiretroviral treatment has resulted in a broad range of clinical complications, including accelerated heart disease. Individuals with HIV infection have a 1.5 to 2 times higher incidence of cardiovascular diseases than their uninfected counterparts; however, the underlying mechanisms are poorly understood. To explore the link between HIV infection and cardiovascular diseases, we used postmortem human heart tissues obtained from HIV-infected and control uninfected individuals to examine connexin 43 (Cx43) expression and distribution and HIV-associated inflammation. Here, we demonstrate that Cx43 is dysregulated in the hearts of HIV-infected individuals. In all HIV heart samples analyzed, there were areas where Cx43 was overexpressed and found along the lateral membrane of the cardiomyocyte and in the intercalated disks. Areas of HIV tissue with anomalous Cx43 expression and localization also showed calcium overload, sarcofilamental atrophy, and accumulation of collagen. All these changes were independent of viral replication, CD4 counts, inflammation, and type of antiretroviral treatment. Overall, we propose that HIV infection increases Cx43 expression in heart, resulting in tissue damage that likely contributes to the high rates of cardiovascular disease in HIV-infected individuals.

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Section: Discussioncontrasting

confidence: 99%

HIV-Associated Cardiovascular Disease

Prevedel

Morocho

Bennett

et al. 2017

The American Journal of Pathology

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“…Our findings are consistent with experimental data showing increased levels of β-catenin in the heart and enhanced production of immunoproteasomes in skeletal muscles of ageing rodents [31,35]. Several previous clinical trials have also demonstrated a positive correlation Table 3.…”

Section: Plos Onesupporting

confidence: 92%

“…To date, only the effect of aging on the content of β-catenin and proteasomal activity in the heart of laboratory animals has been investigated [29,[33][34][35] and only a few clinical trials demonstrating alterations in galectin-3 concentration in the blood of older individuals have been conducted [24,25]. Due to ethical difficulties with obtaining material from healthy people, there are no reports describing changes in the levels of β-catenin, CacyBP/SIP, galectin-3 and proteasome activity in the aging human myocardium.…”

Section: Introductionmentioning

confidence: 99%

Ageing-related changes in the levels of β-catenin, CacyBP/SIP, galectin-3 and immunoproteasome subunit LMP7 in the heart of men

et al. 2020

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Aging is a major risk factor for morbidity and mortality from cardiovascular causes in men. To better understand the cellular processes related to age-related cardiac complications, we undertook research aimed at comparative evaluation of genes expression and distribution of β-catenin, CacyBP/SIP, galectin-3 and LMP7 in the heart of healthy men in different age groups. The study was conducted on the hearts of 12 men (organ donors) without a history of cardiovascular disease, who were divided into two age groups: men under and men over 45 years of age. On paraffin sections, immunohistochemical reactions were performed to detect β-catenin, CacyBP/SIP, galectin-3 and immunoproteasome subunit LMP7. The expression of genes coding β-catenin, CacyBP/SIP, galectin-3 and LMP7 was also evaluated by real-time PCR method. In the heart of men over 45 years old, both gene expression and immunoreactivity of β-catenin, CacyBP/SIP, galectin-3 and LMP7 were stronger compared to younger individuals. The results of the presented studies suggest that β-catenin, CacyBP/SIP, galectin-3 and immunoproteasomes might be involved in the internal regulation of heart homeostasis during ageing.

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“…connexin 43 and β-catenin (β-CAT), N-CAD expression remains unchanged. 52 These data imply that while N-CAD may mechanically regulate differential cell growth (Figure 1, black), other junctional proteins may regulate disease. The catenins, for example, link N-CAD’s cytoplasmic tail to actin via vinculin, and β-CAT in particular changes its localization to the nucleus with age (Figure 1, arrow), 56 mediating fetal gene reactivation through novel transcriptional activity (Figure 1, yellow).…”

Section: Intracellular Remodeling As a Results Of Stress Age Or Diseasementioning

confidence: 94%

“…98 Accumulation of collagen I and collagen III with age has been documented across mammals 52, 53, 99, 100 and including aged healthy human myocardium, suggesting it occurs with physiological aging. 101 While these changes are thought to increase LV tissue stiffness 37 and impair ventricular relaxation, the propensity of data in patients with no known cardiovascular disease suggests that an increase per se is not indicative of pathology.…”

Section: Costamere and Extracellular Matrix Remodeling In Response Tomentioning

confidence: 99%

Mechanical Regulation of Cardiac Aging in Model Systems

Sessions

Engler

2016

Circulation Research

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Unlike diet and exercise, which individuals can modulate according to their lifestyle, aging is unavoidable. With normal or “healthy” aging, the heart undergoes extensive vascular, cellular, and interstitial molecular changes that result in stiffer less compliant hearts that experience a general decline in organ function. While these molecular changes deemed “cardiac remodeling” were once thought to be concomitant with advanced cardiovascular disease, they can be found in patients without manifestation of clinical disease. It is now mostly acknowledged that these age-related mechanical changes confer vulnerability of the heart to cardiovascular stresses associated with disease such as hypertension and atherosclerosis. However, recent studies have aimed at differentiating the initial compensatory changes that occur within the heart with age to maintain contractile function from the maladaptive responses associated with disease. This work has identified new targets to improve cardiac function during aging. Spanning invertebrate to vertebrate models, we use this review to delineate some hallmarks of physiological vs. pathological remodeling that occur in the cardiomyocyte and its microenvironment, focusing especially on the mechanical changes that occur within the sarcomere, intercalated disc, costamere, and extracellular matrix (ECM).

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Remodeling of the intercalated disc related to aging in the mouse heart

Abstract: Our study shows age-related disorganization of ID, which may be responsible for slowed conduction of the depolarization wave within the heart, and supports the hypothesis of cardiac dysfunction in senescence.

Cited by 45 publications

References 42 publications

HIV-Associated Cardiovascular Disease

HIV-Associated Cardiovascular Disease

Ageing-related changes in the levels of β-catenin, CacyBP/SIP, galectin-3 and immunoproteasome subunit LMP7 in the heart of men

Mechanical Regulation of Cardiac Aging in Model Systems

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