Aging and Defective Healing, Adverse Remodeling, and Blunted Post-Conditioning in the Reperfused Wounded Heart⁎⁎Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.

Jugdutt, Bodh I.; Jelani, Anwar

doi:10.1016/j.jacc.2007.12.027

Cited by 22 publications

(4 citation statements)

References 20 publications

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“…With respect to diastolic function, our work is in agreement with that of several other groups who have found a decrease in diastolic function via varying techniques including isolated myocytes (Li et al 2005), isovolumic left heart preparations (Olsson et al 2001) and traditional echocardiography (Przyklenk et al 2008; Scherrer-Crosbie and Kurtz 2010; Taffet et al 1997). Furthermore, Olsson et al (2001) reported a gender and age effect in a transgenic mouse model of familial hypertrophic cardiomyopathy, with males exhibiting earlier and more dramatic decreases in diastolic function and LV cavity dilation, whereas Baumann et al (2008) reported gender- and strain-dependent differences in cardiac function in two different mouse lines using high-resolution echocardiography.…”

Section: Discussionsupporting

confidence: 91%

“…We propose that because age and gender are important factors in human cardiovascular disease, they should be considered in murine studies. Most, but not all (Betsyaku et al 2002; Haghighi et al 2001; Stypmann et al 2006), studies that have examined gender- or age-related changes have found that these factors play a significant role in cardiovascular pathophysiology in both wild-type (Hinton et al 2008; Przyklenk et al 2008) and genetically modified (Bradshaw et al 2010; Dai et al 2009; Olsson et al 2001; Pereira et al 2010; Reddy et al 2007; Yang et al 2008) mice.…”

Section: Introductionmentioning

confidence: 99%

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Age- and Gender-Related Changes in Ventricular Performance in Wild-Type FVB/N Mice as Evaluated by Conventional and Vector Velocity Echocardiography Imaging: A Retrospective Study

Koch¹,

Haworth²,

Robbins³

et al. 2013

Ultrasound in Medicine & Biology

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Detailed studies in animal models to assess the importance of aging animals in cardiovascular research are rather scarce. The increase in mouse models used to study cardiovascular disease makes the establishment of physiologic aging parameters in myocardial function in both male and female mice critical. Forty-four FVB/N mice were studied at multiple time points between the ages of 3 and 16 mo using high-frequency echocardiography. Our study found that there is an age-dependent decrease in several systolic and diastolic function parameters in male mice, but not in female mice. This study establishes the physiologic age- and gender-related changes in myocardial function that occur in mice and can be measured with echocardiography. We report baseline values for traditional echocardiography and advanced echocardiographic techniques to measure discrete changes in cardiac function in the commonly employed FVB/N strain.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Age- and Gender-Related Changes in Ventricular Performance in Wild-Type FVB/N Mice as Evaluated by Conventional and Vector Velocity Echocardiography Imaging: A Retrospective Study

Koch¹,

Haworth²,

Robbins³

et al. 2013

Ultrasound in Medicine & Biology

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“…Finally, a variety of drugs, like anti-inflammatory agents, angiotensin-converting enzyme inhibitors, AT1R blockers, aldosterone and endothelin antagonists, and statins, may also affect healing, impair collagen deposition, and exert adverse effects on myocardial remodelling post injury in the aged population [148][149][150]. Thus, a plethora of senescencerelated defects make the response of cardiac fibroblasts to myocardial injury less effective.…”

Section: Aging and A Poorly Organised Scar In The Injured Heartmentioning

confidence: 99%

The Senescent Heart—“Age Doth Wither Its Infinite Variety”

Vijayakumar,

Wang,

Kailasam

2024

IJMS

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Cardiovascular diseases are a leading cause of morbidity and mortality world-wide. While many factors like smoking, hypertension, diabetes, dyslipidaemia, a sedentary lifestyle, and genetic factors can predispose to cardiovascular diseases, the natural process of aging is by itself a major determinant of the risk. Cardiac aging is marked by a conglomerate of cellular and molecular changes, exacerbated by age-driven decline in cardiac regeneration capacity. Although the phenotypes of cardiac aging are well characterised, the underlying molecular mechanisms are far less explored. Recent advances unequivocally link cardiovascular aging to the dysregulation of critical signalling pathways in cardiac fibroblasts, which compromises the critical role of these cells in maintaining the structural and functional integrity of the myocardium. Clearly, the identification of cardiac fibroblast-specific factors and mechanisms that regulate cardiac fibroblast function in the senescent myocardium is of immense importance. In this regard, recent studies show that Discoidin domain receptor 2 (DDR2), a collagen-activated receptor tyrosine kinase predominantly located in cardiac fibroblasts, has an obligate role in cardiac fibroblast function and cardiovascular fibrosis. Incisive studies on the molecular basis of cardiovascular aging and dysregulated fibroblast function in the senescent heart would pave the way for effective strategies to mitigate cardiovascular diseases in a rapidly growing elderly population.

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“…Cardiac myofibroblasts more effectively secrete and remodel ECM fibrous proteins and proteoglycans and provoke a gradual accumulation of ECM proteins in the interstitium; these adjustments lead to perivascular, endomysial, and perimysial fibrosis. [88, 89]. Thus, in many ways, myofibroblasts emerge as the effectors of transition to disease through overcompensation which leads to the establishment of a fibrogenic milieu.…”

Section: Pathological Hypertrophy In Cavdmentioning

confidence: 99%

Calcific Aortic Valve Disease: Part 2—Morphomechanical Abnormalities, Gene Reexpression, and Gender Effects on Ventricular Hypertrophy and Its Reversibility

Pasipoularides

2016

J. of Cardiovasc. Trans. Res.

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In part 1, we considered cytomolecular mechanisms underlying calcific aortic valve disease (CAVD), hemodynamics, and adaptive feedbacks controlling pathological left ventricular hypertrophy provoked by ensuing aortic valvular stenosis (AVS). In part 2, we survey diverse signal transduction pathways that precede cellular/molecular mechanisms controlling hypertrophic gene expression by activation of specific transcription factors that induce sarcomere replication in-parallel. Such signaling pathways represent potential targets for therapeutic intervention and prevention of decompensation/failure. Hypertrophy provoking signals, in the form of dynamic stresses and ligand/effector molecules that bind to specific receptors to initiate the hypertrophy, are transcribed across the sarcolemma by several second messengers. They comprise intricate feedback mechanisms involving gene network cascades, specific signaling molecules encompassing G protein-coupled receptors and mechanotransducers, and myocardial stresses. Future multidisciplinary studies will characterize the adaptive/maladaptive nature of the AVS-induced hypertrophy, its gender- and individual patient-dependent peculiarities, and its response to surgical/medical interventions. They will herald more effective, precision medicine treatments.

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Cited by 22 publications

References 20 publications

Age- and Gender-Related Changes in Ventricular Performance in Wild-Type FVB/N Mice as Evaluated by Conventional and Vector Velocity Echocardiography Imaging: A Retrospective Study

Age- and Gender-Related Changes in Ventricular Performance in Wild-Type FVB/N Mice as Evaluated by Conventional and Vector Velocity Echocardiography Imaging: A Retrospective Study

The Senescent Heart—“Age Doth Wither Its Infinite Variety”

Calcific Aortic Valve Disease: Part 2—Morphomechanical Abnormalities, Gene Reexpression, and Gender Effects on Ventricular Hypertrophy and Its Reversibility

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