Plasma and Myocardial miRNomes Similarities and Differences during Cardiac Remodelling and Reverse Remodelling in a Murine Model of Heart Failure with Preserved Ejection Fraction DOI Creative Commons

Sara-Ève Thibodeau,

Emylie-Ann Labbé,

Élisabeth Walsh‐Wilkinson

и другие.

Biomolecules, Год журнала: 2024, Номер 14(8), С. 892 - 892

Опубликована: Июль 24, 2024

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome characterised by multiple risk factors touching various organs outside the heart. Using murine HFpEF model, we studied cardiac reverse remodelling (RR) after stopping causing metabolic-hypertensive stress (MHS; Angiotensin II [AngII] and high-fat diet [HFD]) 28 days introducing voluntary exercise (VE) for four more weeks. We measured effects of MHS RR on plasma myocardial microRNA (miR) profile (miRNome) to characterise better non-cardiac responses HFpEF-inducing their reversibility. AngII alone, HFD or caused hypertrophy (CH), left ventricular (LV) concentric atrial enlargement in females. Only MHS, but not HFD, did males. After RR, CH, LV were normalised. Among 25 most abundant circulating miRs, 10 modulated MHS. Plasma miRNomes from AngII, mice shared 31 common significantly miRs (24 upregulated 7 downregulated), suggesting that response producing bulk those was similar even seemingly different stress. In LV, 19 out expressed modulated. restored normality miRNome miRNome, which remained mostly unchanged. Our results suggest abnormalities persist myocardium normalisation circulatory markers may be falsely reassuring recovery.

Язык: Английский

Heart failure with preserved ejection fraction and atrial fibrillation: epidemiology, pathophysiology, and diagnosis interplay DOI
Veraprapas Kittipibul, Carolyn S.P. Lam

Heart Failure Reviews, Год журнала: 2025, Номер unknown

Опубликована: Янв. 24, 2025

Язык: Английский

Процитировано

2
Nrf2-Keap1 in Cardiovascular Disease: Which Is the Cart and Which the Horse? DOI
Neha Dhyani, Changhai Tian, Lie Gao

и другие.

Physiology, Год журнала: 2024, Номер 39(5), С. 288 - 301

Опубликована: Апрель 30, 2024

High levels of oxidant stress in the form reactive species are prevalent circulation and tissues various types cardiovascular disease including heart failure, hypertension, peripheral arterial disease, stroke. Here we review role nuclear factor erythroid 2-related 2 (Nrf2), an important widespread antioxidant anti-inflammatory transcription that may contribute to pathogenesis maintenance diseases. We studies showing downregulation Nrf2 exacerbates autonomic function. Finally, discuss potential for using modulation as a therapeutic strategy diseases dysfunction.

Язык: Английский

Процитировано

5
The synergistic role of gut microbiota and RNA in metabolic diseases: mechanisms and therapeutic insights DOI Creative Commons
Zhuo Huang, Qinyan Yao,

Shuang Ma

и другие.

Frontiers in Microbiology, Год журнала: 2025, Номер 16

Опубликована: Янв. 29, 2025

The gut microbiota plays a pivotal role in human metabolic health by influencing immune responses, digestion, and homeostasis. Recent research highlights the intricate interactions between RNA, especially non-coding RNAs, regulating processes. Dysbiosis of has been linked to disorders such as type 2 diabetes, obesity, metabolic-associated fatty liver disease (MAFLD) heart disease. Microbial metabolites, including short-chain acids (SCFAs), modulate RNA expression, lipid metabolism, glucose regulation, inflammatory responses. Additionally, microRNAs (miRNAs) long RNAs (lncRNAs) serve critical regulators these processes, with emerging evidence showing that gut-derived metabolites affect post-transcriptional gene regulation. This review synthesizes current understanding microbiota-RNA axis its diseases. By exploring molecular mechanisms, particularly how microbiota-derived signals pathways, underscores potential targeting this for therapeutic interventions. Furthermore, it examines dysbiosis leads epigenetic changes m6A methylation, contributing pathogenesis. These insights offer new perspective on prevention treatment diseases, applications personalized medicine.

Язык: Английский

Процитировано

0
Atrial Fibrillation (AF) and Heart Failure With Preserved Ejection Fraction (HFpEF): Advances and Challenges DOI Creative Commons
Sanjeev Saksena, April Slee,

Ranghadham Nagarakanti

и другие.

Journal of Cardiovascular Electrophysiology, Год журнала: 2025, Номер unknown

Опубликована: Март 10, 2025

This state-of-the-art review is based on the Philippe Coumel Lecture in 2024 (Figure 1). It highlights confluence of two major cardiovascular epidemics, atrial fibrillation and heart failure, with preserved ejection fraction. In these conditions, advances electrophysiology failure physiology are intertwined integrated this review. constellation disease states has its own unique epidemiologic features, pathophysiology, experimental clinical mechanisms; an increasing knowledge base respect to presentation, prognostic implications, therapeutic options from pharmacologic non-pharmacologic interventions. Major advances, continuing challenges, future directions condition described rapidly evolving field scientific endeavor.

Язык: Английский

Процитировано

0
Circulating Non-Coding RNAs as Indicators of Fibrosis and Heart Failure Severity DOI Creative Commons

Veronika Boichenko,

Victoria Maria Noakes,

Benedict Reilly-O’Donnell

и другие.

Cells, Год журнала: 2025, Номер 14(7), С. 553 - 553

Опубликована: Апрель 7, 2025

Heart failure (HF) is a leading cause of morbidity and mortality worldwide, representing complex clinical syndrome in which the heart’s ability to pump blood efficiently impaired. HF can be subclassified into heart with reduced ejection fraction (HFrEF) preserved (HFpEF), each distinct pathophysiological mechanisms varying levels severity. The progression significantly driven by cardiac fibrosis, pathological process extracellular matrix undergoes abnormal uncontrolled remodelling. Cardiac fibrosis characterized excessive protein deposition activation myofibroblasts, increasing stiffness heart, thus disrupting its normal structure function promoting lethal arrythmia. MicroRNAs, long non-coding RNAs, circular collectively known as RNAs (ncRNAs), have recently gained significant attention due growing body evidence suggesting their involvement remodelling such fibrosis. ncRNAs found peripheral blood, indicating potential biomarkers for assessing In this review, we critically examine recent advancements findings related use discuss implication development.

Язык: Английский

Процитировано

0
Plasma and Myocardial miRNomes Similarities and Differences during Cardiac Remodelling and Reverse Remodelling in a Murine Model of Heart Failure with Preserved Ejection Fraction DOI Open Access

Sara-Ève Thibodeau,

Emylie-Ann Labbé,

Élisabeth Walsh‐Wilkinson

и другие.

Опубликована: Июнь 27, 2024

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome characterized by multiple risk factors and associated conditions. HFpEF prevalence rising, its prognosis remains poor after the first hospitalization. Using two-hit murine model, we aimed at studying cardiac reverse remodelling stopping causing stress (Angiotensin II [AngII]) high-fat diet [HFD]; MHS) introducing voluntary exercise. We studied in young male female C57Bl6/J mice fed or not an HFD (60% calories from fat) response to AngII (1.5 mg/kg/day for 28 days). Then, MHS was stopped, VE started another four weeks (RR). effects of RR on circulatory microRNA (miR) profile (miRNome) myocardial miRNome characterize non-cardiac small RNAs. alone but caused hypertrophy (CH), left ventricular (LV) concentric atrial enlargement mice. HFD-induced CH LV only Four RR, CH, were reversed. performed bulk miR sequencing. did observe differences linked biological sex. restored normality miRNome, whereas remained relatively similar one MHS. Among 25 most abundant miRs, ten modulated (9 upregulated). In LV, 8 upregulated MHS, 10 downregulated. MiRNomes AngII, shared many common miRs (32), suggesting that overall organs producing non-coding RNA even seemingly different stress.

Язык: Английский

Процитировано

1
Divergent cardiac and renal effects of miR-181c-5p inhibition in a rodent heart failure model DOI Creative Commons
Jente R. A. Boen, Andreas B. Gevaert, Amélie Dendooven

и другие.

Frontiers in Cardiovascular Medicine, Год журнала: 2024, Номер 11

Опубликована: Апрель 25, 2024

Aims MiR-181c-5p overexpression associates with heart failure (HF) and cardiac damage, but the underlying pathophysiology remains unclear. This study investigated effect of miR-181c-5p inhibition on function fibrosis in a rodent model diastolic dysfunction, evaluated additional effects kidney as relevant comorbid organ. Methods results Diastolic dysfunction was induced male C57/BL6J mice ( n = 20) by combining high-fat diet, L-NG-nitroarginine methyl ester, angiotensin II administration, compared to sham controls 18). Mice were randomized subcutaneous antagomiR (INH) or scrambled injections (40 mg/kg/week). HF demonstrated increased fibrosis, which attenuated INH treatment. Remarkably, + animals had threefold higher mortality rate (60%) (20%). Histological examination revealed glomerular damage all treated mice, signs thrombotic microangiopathy (TMA) who died prematurely. Quantitative polymerase chain reaction miR-181c-5p-related downregulation not renal Tgfbr1 while treatment reduced Vegfa expression mice. Conclusion demonstrates anti-fibrotic through targeting heart. Despite improved function, due predisposition for TMA, associated kidneys.

Язык: Английский

Процитировано

0
Plasma and Myocardial miRNomes Similarities and Differences during Cardiac Remodelling and Reverse Remodelling in a Murine Model of Heart Failure with Preserved Ejection Fraction DOI Creative Commons

Sara-Ève Thibodeau,

Emylie-Ann Labbé,

Élisabeth Walsh‐Wilkinson

и другие.

Biomolecules, Год журнала: 2024, Номер 14(8), С. 892 - 892

Опубликована: Июль 24, 2024

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome characterised by multiple risk factors touching various organs outside the heart. Using murine HFpEF model, we studied cardiac reverse remodelling (RR) after stopping causing metabolic-hypertensive stress (MHS; Angiotensin II [AngII] and high-fat diet [HFD]) 28 days introducing voluntary exercise (VE) for four more weeks. We measured effects of MHS RR on plasma myocardial microRNA (miR) profile (miRNome) to characterise better non-cardiac responses HFpEF-inducing their reversibility. AngII alone, HFD or caused hypertrophy (CH), left ventricular (LV) concentric atrial enlargement in females. Only MHS, but not HFD, did males. After RR, CH, LV were normalised. Among 25 most abundant circulating miRs, 10 modulated MHS. Plasma miRNomes from AngII, mice shared 31 common significantly miRs (24 upregulated 7 downregulated), suggesting that response producing bulk those was similar even seemingly different stress. In LV, 19 out expressed modulated. restored normality miRNome miRNome, which remained mostly unchanged. Our results suggest abnormalities persist myocardium normalisation circulatory markers may be falsely reassuring recovery.

Язык: Английский

Процитировано

0