Gender and Aging Lead to Myocardial Fibrosis DOI

云会 王

Advances in Clinical Medicine, Journal Year: 2022, Volume and Issue: 12(11), P. 10026 - 10033

Published: Jan. 1, 2022

Language: Английский

Hearts apart: sex differences in cardiac remodeling in health and disease DOI Creative Commons
Thomas G. Martin, Leslie A. Leinwand

Journal of Clinical Investigation, Journal Year: 2024, Volume and Issue: 134(13)

Published: June 30, 2024

Biological sex is an important modifier of physiology and influences pathobiology in many diseases. While heart disease the number one cause death worldwide both men women, differences exist at organ cellular scales, affecting clinical presentation, diagnosis, treatment. In this Review, we highlight baseline cardiac structure, function, signaling discuss contribution hormones chromosomes to these characteristics. The a remarkably plastic rapidly responds physiological pathological cues by modifying form function. nature extent remodeling response stimuli are often dependent on biological sex. We organ- molecular-level adaptive from pressure volume overload, ischemia, genetic disease. Finally, offer perspective key future directions for research into differences.

Language: Английский

Citations

18

Extracellular Matrix Dynamics as an Emerging yet Understudied Hallmark of Aging and Longevity DOI Creative Commons
Cyril Statzer,

Ji Young Cecilia Park,

Collin Y. Ewald

et al.

Aging and Disease, Journal Year: 2023, Volume and Issue: 14(3), P. 670 - 670

Published: Jan. 1, 2023

The biomechanical properties of extracellular matrices (ECM) and their consequences for cellular homeostasis have recently emerged as a driver aging. Here we review the age-dependent deterioration ECM in context our current understanding aging processes. We discuss reciprocal interactions longevity interventions with remodeling. And relevance dynamics captured by matrisome matreotypes associated health, disease, longevity. Furthermore, highlight that many established compounds promote homeostasis. A large body evidence to qualify hallmark is emerging, data invertebrates promising. However, direct experimental proof activating sufficient slow mammals lacking. conclude further research required anticipate conceptual framework biomechanics will provide new strategies health during

Language: Английский

Citations

40

Sex-specific molecular drivers of cardiac fibrosis in aging hearts DOI

Katie Anne Fopiano,

Márta Balogh,

Vijay Patel

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: March 2, 2025

Language: Английский

Citations

1

Cardiac aging: from hallmarks to therapeutic opportunities DOI Creative Commons
Margaret H. Hastings, Qiulian Zhou, Chao Wu

et al.

Cardiovascular Research, Journal Year: 2024, Volume and Issue: unknown

Published: June 26, 2024

Abstract Cardiac ageing is an intricate and multifaceted process with considerable impact on public health, especially given the global demographic shift towards aged populations. This review discusses structural, cellular, functional changes associated cardiac heart failure preserved ejection fraction (HFpEF). Key molecular mediators are considered within framework of established hallmarks ageing, particular attention to promising therapeutic candidates. We further delineate differential impacts structure function in men women, addressing hormonal chromosomal influences. The protective mitigating effects exercise HFpEF discussed, as inspiration for identification pathways that mitigate biological ageing. also emphasize how much remains be learned importance these efforts enhancing health populations worldwide.

Language: Английский

Citations

7

Myocardial fibrosis from the perspective of the extracellular matrix: mechanisms to clinical impact DOI
Ida G. Lunde, Karoline Bjarnesdatter Rypdal, Sophie Van Linthout

et al.

Matrix Biology, Journal Year: 2024, Volume and Issue: 134, P. 1 - 22

Published: Aug. 29, 2024

Language: Английский

Citations

7

Regulator of G-Protein Signaling-4 Attenuates Cardiac Adverse Remodeling and Neuronal Norepinephrine Release-Promoting Free Fatty Acid Receptor FFAR3 Signaling DOI Open Access
Alexandra Carbone,

Jordana I. Borges,

Malka S. Suster

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(10), P. 5803 - 5803

Published: May 22, 2022

Propionic acid is a cell nutrient but also stimulus for cellular signaling. Free fatty receptor (FFAR)-3, known as GPR41, Gi/o protein-coupled (GPCR) that mediates some of the propionate's actions in cells, such inflammation, fibrosis, and increased firing/norepinephrine release from peripheral sympathetic neurons. The regulator G-protein Signaling (RGS)-4 inactivates (terminates) both Gi/o- Gq-protein signaling and, heart, protects against atrial fibrillation via calcium attenuation. RGS4 activity stimulated by β-adrenergic receptors (ARs) protein kinase A (PKA)-dependent phosphorylation. Herein, we examined whether modulates cardiac FFAR3 signaling/function. We report essential dampening H9c2 cardiomyocytes, since siRNA-mediated depletion significantly enhanced propionate-dependent cAMP lowering, activation, p38 MAPK pro-inflammatory interleukin (IL)-1β IL-6 production, pro-fibrotic transforming growth factor (TGF)-β synthesis. Additionally, catecholamine pretreatment blocked propionic acid/FFAR3 PKA-dependent activation cardiomyocytes. Finally, opposes FFAR3-dependent norepinephrine sympathetic-like neurons (differentiated Neuro-2a cells) co-cultured with thereby preserving functional βAR number In conclusion, appears propionate/FFAR3 attenuation cardiomyocytes neurons, leading to cardioprotection inflammation/adverse remodeling sympatholysis, respectively.

Language: Английский

Citations

26

Sex-specific structural and functional cardiac remodeling during healthy aging assessed by cardiovascular magnetic resonance DOI Creative Commons

Leonhard Grassow,

Jan Gröschel,

Hadil Saad

et al.

Clinical Research in Cardiology, Journal Year: 2024, Volume and Issue: unknown

Published: March 11, 2024

Abstract Background Aging as a major non-modifiable cardiac risk factor challenges future cardiovascular medicine and economic demands, which requires further assessments addressing physiological age-associated changes. Objectives Using magnetic resonance (CMR), this study aims to characterize sex-specific ventricular adaptations during healthy aging. Methods The population included volunteers who underwent CMR at 1.5 or 3 Tesla scanners applying cine-imaging with short-axis coverage of the left (LV) right (RV) ventricle. cohort was divided by sex (female male) age (subgroups in years): 1 (19–29), 2 (30–39), (40–49), 4 (≥50). Cardiac were quantitatively assessed indices. Results After exclusion missing poor-quality datasets diagnosed disease, 140 203 part final analysis. Women generally had smaller dimensions LV mass, but higher biventricular systolic function. There significant decrease well increase mass-to-volume ratio (LV-MVR, concentricity) both sexes (LV-MVR g/ml: group vs. 4: females 0.50 0.57, p =0.016, males 0.56 0.67, =0.024). stroke volume index decreased significantly sexes, stronger for men than women (in ml/m : 51.76 41.94, <0.001, 55.31 40.78, <0.001). Ventricular proportions (RV-to-LV-volume ratio) constant between groups sexes. Conclusions In aging associated an concentricity decline dimensions. Furthermore, relevant age-related differences performance observed. Graphical ↓, decrease; ↑, increase; ±, maintaining. Abbreviations: CMR, resonance; EDV, end-diastolic volume; EF, ejection fraction; LV, ventricle; MVR, ratio; RV, SVI, index; T, Tesla; VR, ratio.

Language: Английский

Citations

4

Circadian biology of cardiac aging DOI

Sharanya S. Bettadapura,

William D. Todd, Graham R. McGinnis

et al.

Journal of Molecular and Cellular Cardiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0

Sex-chromosome mechanisms in cardiac development and disease DOI
Frank L. Conlon, Arthur P. Arnold

Nature Cardiovascular Research, Journal Year: 2023, Volume and Issue: 2(4), P. 340 - 350

Published: April 3, 2023

Language: Английский

Citations

10

Circulated TGF-β1 and VEGF-A as Biomarkers for Fabry Disease-Associated Cardiomyopathy DOI Creative Commons
Margarita M. Ivanova,

Julia Dao,

Omar Abu Slayeh

et al.

Cells, Journal Year: 2023, Volume and Issue: 12(16), P. 2102 - 2102

Published: Aug. 19, 2023

Fabry disease (FD) is a lysosomal disorder caused by α-galactosidase A deficiency, resulting in the accumulation of globotriaosylceramide (Gb-3) and its metabolite globotriaosylsphingosine (Lyso-Gb-3). Cardiovascular complications hypertrophic cardiomyopathy (HCM) are most frequent manifestations FD. While an echocardiogram cardiac MRI clinical tools to assess involvement, pattern variations fibrosis make it crucial identify biomarkers predict early outcomes. This study aims investigate potential associated with HCM FD: transforming growth factor-β1 (TGF-β1), TGF-β active form (a-TGF-β), vascular endothelial factor (VEGF-A), fibroblast (FGF2) 45 patients FD, categorized into cohorts based on severity. TGF-β1, a-TGF-β, FGF2, VEGF-A were elevated association TGF-β1 was not gender-related, VEGF males FD HCM. Female abnormal electrocardiograms but without overt also have TGF-β1. Lyso-Gb3 correlated VEGF-A, a-TGF-β1. Elevation provides evidence chronic inflammatory state as cause myocardial patients; thus, marker detected even prior hypertrophy. may be prognostic indicators adverse cardiovascular events

Language: Английский

Citations

8