Modern Concepts in Cardiovascular Disease: Inflamm-Aging

Puspitasari, Yustina M.; Ministrini, Stefano; Schwarz, Lena; Karch, Cristoph; Liberale, Luca; Camici, Giovanni G.

doi:10.3389/fcell.2022.882211

Cited by 24 publications

(15 citation statements)

References 155 publications

(186 reference statements)

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“…Consistently, prior research has shown that CD73 produces adenosine acutely during injury as a homeostatic response to the increased cardiac inflammation; however, its excessive production can promote tissue damage [ 37 , 38 ]. Furthermore, in correlation with the extent of cardiomyocyte necrosis, studies have reported that cardiomyocyte necrosis following injury aggravates proinflammatory responses [ 39 , 40 ]. In contrast to E2 deficiency, E2 Endo presence (in SHAM + ISO) and E2 Exo supplementation (in OVX + E2 + ISO) significantly decreased CD73/adenosine hyperactivity.…”

Section: Discussionmentioning

confidence: 99%

Estrogen downregulates CD73/adenosine axis hyperactivity via adaptive modulation PI3K/Akt signaling to prevent myocarditis and arrhythmias during chronic catecholamines stress

et al. 2023

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Background During myocardial damage, the sex hormone estrogen and CD73, the main enzyme that converts AMP into adenosine, are cardioprotective molecules. However, it is unclear how these two molecules work together to provide cardioprotection. The current study aimed to elucidate the interaction between estrogen and CD73 under chronic stress. Methods Ovariectomy and SHAM operations were done on FVB wild-type (WT) female mice. Two weeks after the operation, the mice were treated with daily isoproterenol (10 mg/kg/day) injections for 14 days. The effect of E2 on relevant cardiac injury biomarkers (BNP, ANP), myocardial morphology (cardiomyocyte surface area), electrocardiography, CD73 protein expression and activity, and macrophage (CD86 + and CD206 +) infiltrations were assessed. In vitro, H9C2 cells were treated with 1 nM of estrogen and 10 mM APCP (CD73 inhibitor α, β-methylene adenosine-5'-diphosphate), 10 µM isoproterenol and 20 µm LY294002 (PI3K inhibitor) for 24 h and western blot was done to elucidate the mechanism behind the effect of estrogen on the CD73/adenosine axis. Results Estrogen deficiency during chronic catecholamine stress caused myocardial injury, thereby triggering the hyperactivity of the CD73/adenosine axis, which aggravated myocarditis, adverse remodeling, and arrhythmias. However, estrogen normalizes CD73/Adenosine axis via the upregulation of PI3K/Akt pathways to prevent adverse outcomes during stress. In vivo results showed that the inhibition of PI3K significantly decreased PI3K/Akt pathways while upregulating the CD73/adenosine axis and apoptosis. Conclusion Estrogen’s pleiotropy cardioprotection mechanism during stress includes its normalization of the CD73/Adenosine axis via the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Estrogen downregulates CD73/adenosine axis hyperactivity via adaptive modulation PI3K/Akt signaling to prevent myocarditis and arrhythmias during chronic catecholamines stress

et al. 2023

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“…In this direction, attention has been drawn toward inflamm-aging. Inflamm-aging, which is characterized by chronic low-grade inflammation during aging, has been linked to various age-related diseases [ 95 ]. This phenomenon involves the presence of systemic inflammatory mediators in elderly individuals, which can exacerbate immune system disturbances and contribute to the development of several persistent diseases.…”

Section: Future Directions and Emerging Trendsmentioning

confidence: 99%

Exploring the Landscape of Anti-Inflammatory Trials: A Comprehensive Review of Strategies for Targeting Inflammation in Acute Myocardial Infraction

Mitsis,

Kyriakou,

Sokratous

et al. 2024

Biomedicines

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The role of inflammation in the pathophysiology of acute myocardial infarction (AMI) is well established. In recognizing inflammation’s pivotal role in AMI, this manuscript systematically traces the historical studies spanning from early attempts to the present landscape. Several anti-inflammatory trials targeting inflammation in post-AMI have been performed, and this review includes the key trials, as well as examines their designs, patient demographics, and primary outcomes. Efficacies and challenges are analyzed, thereby shedding light on the translational implications of trial outcomes. This article also discusses emerging trends, ongoing research, and potential future directions in the field. Practical applications and implications for clinical practice are considered by providing a holistic view of the evolving landscape of anti-inflammatory interventions in the context of AMI.

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“…This pro-inflammatory milieu perpetuates the chronic low-grade inflammation commonly seen in aging. This figure was modified from Puspitasari et al [ 69 ] . Additionally, the figure was prepared using Biorender, https://biorender.com/ ).…”

Section: Figurementioning

confidence: 99%

Immune mechanisms of cardiac aging

2023

J Cardiovasc Aging

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Advances in healthcare and improvements in living conditions have led to rising life expectancy worldwide. Aging is associated with excessive oxidative stress, a chronic inflammatory state, and limited tissue healing, all of which result in an increased risk of heart failure. In fact, the prevalence of heart failure approaches 40% in the ninth decade of life, with the majority of these cases suffering from heart failure with preserved ejection fraction (HFpEF). In cardiomyocytes (CMs), age-related mitochondrial dysfunction results in disrupted calcium signaling and covalent protein-linked aggregates, which cause cardiomyocyte functional disturbances, resulting in increased stiffness and diastolic dysfunction. Importantly, aging is also associated with chronic low-grade, sterile inflammation, which alters the function of interstitial cardiac cells and leads to cardiac fibrosis. Taken together, cardiac aging is associated with cellular, structural, and functional changes in the heart that contribute to the rising prevalence of heart failure in older people.

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Modern Concepts in Cardiovascular Disease: Inflamm-Aging

Cited by 24 publications

References 155 publications

Estrogen downregulates CD73/adenosine axis hyperactivity via adaptive modulation PI3K/Akt signaling to prevent myocarditis and arrhythmias during chronic catecholamines stress

Estrogen downregulates CD73/adenosine axis hyperactivity via adaptive modulation PI3K/Akt signaling to prevent myocarditis and arrhythmias during chronic catecholamines stress

Exploring the Landscape of Anti-Inflammatory Trials: A Comprehensive Review of Strategies for Targeting Inflammation in Acute Myocardial Infraction

Immune mechanisms of cardiac aging

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