Sex/Gender-Specific Imbalance in CVD: Could Physical Activity Help to Improve Clinical Outcome Targeting CVD Molecular Mechanisms in Women? DOI Open Access
Mauro Vaccarezza, Verónica Papa, Daniela Milani

et al.

International Journal of Molecular Sciences, Journal Year: 2020, Volume and Issue: 21(4), P. 1477 - 1477

Published: Feb. 21, 2020

In the last two decades, new insights have been gained regarding sex/gender-related differences in cardiovascular disease (CVD). CVD represents leading cause of death worldwide both men and women, accounting for at least one-third all deaths women half over 50 years developing countries. Important sex-related prevalence, presentation, management, outcomes different CVDs recently discovered, demonstrating sex/gender-specific pathophysiologic features presentation prognosis women. A large amount evidence has highlighted role sex hormones protecting from CVDs, providing an advantage that is lost when reach menopause stage. This hormonal-dependent shift risk consequently affects overall epidemiology, particularly light increasing trend population aging. The benefits physical activity recognized a long time as powerful preventive approach prevention aging-related morbidity control. Exercise training indeed potent physiological stimulus, which reduces primary secondary events. However, underlying mechanisms these positive effects, including sex/gender perspective, still need to be fully elucidated. aim this work provide review linking CVD, molecular mediators, explore whether sex- gender-tailored may used effective tool prevent improve clinical

Language: Английский

Lifestyle, Oxidative Stress, and Antioxidants: Back and Forth in the Pathophysiology of Chronic Diseases DOI Creative Commons
Mehdi Sharifi‐Rad, N. V. Anil Kumar, Paolo Zucca

et al.

Frontiers in Physiology, Journal Year: 2020, Volume and Issue: 11

Published: July 2, 2020

Oxidative stress plays an essential role in the pathogenesis of chronic diseases such as cardiovascular diseases, diabetes, neurodegenerative and cancer. Long term exposure to increased levels pro-oxidant factors can cause structural defects at a mitochondrial DNA level, well functional alteration several enzymes cellular structures leading aberrations gene expression. The modern lifestyle associated with processed food, wide range chemicals lack exercise important oxidative induction. However, use medicinal plants antioxidant properties has been exploited for their ability treat or prevent human pathologies which seems be one causes. In this review we discuss is triggers plant-derived compounds mechanisms defenses that help prevention these diseases. Finally, both beneficial detrimental effects molecules are used reduce conditions discussed.

Language: Английский

Citations

1520
Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases DOI
Jun Ren, Yaguang Bi, James R. Sowers

et al.

Nature Reviews Cardiology, Journal Year: 2021, Volume and Issue: 18(7), P. 499 - 521

Published: Feb. 22, 2021

Language: Английский

Citations

482
Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications DOI
Jun Ren, Ne N. Wu, Shuyi Wang

et al.

Physiological Reviews, Journal Year: 2021, Volume and Issue: 101(4), P. 1745 - 1807

Published: May 5, 2021

The prevalence of heart failure is on the rise and imposes a major health threat, in part, due to rapidly increased overweight obesity. To this point, epidemiological, clinical, experimental evidence supports existence unique disease entity termed "obesity cardiomyopathy," which develops independent hypertension, coronary disease, other diseases. Our contemporary review evaluates for pathological condition, examines putative responsible mechanisms, discusses therapeutic options disorder. Clinical findings have consolidated presence left ventricular dysfunction Experimental investigations uncovered pathophysiological changes myocardial structure function genetically predisposed diet-induced Indeed, consolidates wide array cellular molecular mechanisms underlying etiology obesity cardiomyopathy including adipose tissue dysfunction, systemic inflammation, metabolic disturbances (insulin resistance, abnormal glucose transport, spillover free fatty acids, lipotoxicity, amino acid derangement), altered intracellular especially mitochondrial Ca2+ homeostasis, oxidative stress, autophagy/mitophagy defect, fibrosis, dampened flow reserve, microvascular (microangiopathy), endothelial impairment. Given important role risk failure, that with preserved systolic recent rises COVID-19-associated cardiovascular mortality, should provide compelling cardiomyopathy, various comorbid conditions, offer new insights into potential approaches (pharmacological lifestyle modification) clinical management cardiomyopathy.

Language: Английский

Citations

253
Targeting autophagy in ischemic stroke: From molecular mechanisms to clinical therapeutics DOI Creative Commons
Amir Ajoolabady,

Shuyi Wang,

Guido Kroemer

et al.

Pharmacology & Therapeutics, Journal Year: 2021, Volume and Issue: 225, P. 107848 - 107848

Published: April 4, 2021

Language: Английский

Citations

217
Mitophagy in Human Diseases DOI Open Access
Laura Doblado,

Claudia Lueck,

Claudia Rey

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(8), P. 3903 - 3903

Published: April 9, 2021

Mitophagy is a selective autophagic process, essential for cellular homeostasis, that eliminates dysfunctional mitochondria. Activated by inner membrane depolarization, it plays an important role during development and fundamental in highly differentiated post-mitotic cells are dependent on aerobic metabolism, such as neurons, muscle cells, hepatocytes. Both defective excessive mitophagy have been proposed to contribute age-related neurodegenerative diseases, Parkinson’s Alzheimer’s metabolic vascular complications of diabetes, myocardial injury, dystrophy, liver disease, among others. Pharmacological or dietary interventions restore homeostasis facilitate the elimination irreversibly damaged mitochondria, thus, could serve potential therapies several chronic diseases. However, despite extraordinary advances this field, mainly derived from vitro preclinical animal models, human applications based regulation mitochondrial quality patients not yet approved. In review, we summarize key autophagy pathways their prevalent diseases highlight use specific interventions.

Language: Английский

Citations

168
FUNDC1 insufficiency sensitizes high fat diet intake-induced cardiac remodeling and contractile anomaly through ACSL4-mediated ferroptosis DOI

Zhaohui Pei,

Yandong Liu, Suqin Liu

et al.

Metabolism, Journal Year: 2021, Volume and Issue: 122, P. 154840 - 154840

Published: July 29, 2021

Language: Английский

Citations

117
Mitophagy inhibitor liensinine suppresses doxorubicin-induced cardiotoxicity through inhibition of Drp1-mediated maladaptive mitochondrial fission DOI
Xinyue Liang, Shuyi Wang, Lifeng Wang

et al.

Pharmacological Research, Journal Year: 2020, Volume and Issue: 157, P. 104846 - 104846

Published: April 25, 2020

Language: Английский

Citations

123
Mitochondrial Ca2+ regulation in the etiology of heart failure: physiological and pathophysiological implications DOI Open Access
Haixia Xu,

Sumei Cui,

Yingmei Zhang

et al.

Acta Pharmacologica Sinica, Journal Year: 2020, Volume and Issue: 41(10), P. 1301 - 1309

Published: July 21, 2020

Language: Английский

Citations

82
ER Stress in Cardiometabolic Diseases: From Molecular Mechanisms to Therapeutics DOI Open Access
Amir Ajoolabady, Shuyi Wang, Guido Kroemer

et al.

Endocrine Reviews, Journal Year: 2021, Volume and Issue: 42(6), P. 839 - 871

Published: March 8, 2021

The endoplasmic reticulum (ER) hosts linear polypeptides and fosters natural folding of proteins through ER-residing chaperones enzymes. Failure the ER to align compose proper protein architecture leads accumulation misfolded/unfolded in lumen, which disturbs homeostasis provoke stress. Presence stress initiates cytoprotective unfolded response (UPR) restore or instigates a rather maladaptive UPR promote cell death. Although wide array cellular processes such as persistent autophagy, dysregulated mitophagy, secretion proinflammatory cytokines may contribute onset progression cardiometabolic diseases, it is well perceived that also evokes development particularly cardiovascular diseases (CVDs), diabetes mellitus, obesity, chronic kidney disease (CKD). Meanwhile, these pathological conditions further aggravate stress, creating vicious cycle. Here this review, we aimed at summarizing updating available information on CVDs, CKD, hoping offer novel insights for management comorbidities regulation

Language: Английский

Citations

63
Physical activity, cardiorespiratory fitness, and cardiovascular health: A clinical practice statement of the American Society for Preventive Cardiology Part I: Bioenergetics, contemporary physical activity recommendations, benefits, risks, extreme exercise regimens, potential maladaptations DOI Creative Commons
Barry A. Franklin, Thijs M.H. Eijsvogels, Ambarish Pandey

et al.

American Journal of Preventive Cardiology, Journal Year: 2022, Volume and Issue: 12, P. 100424 - 100424

Published: Oct. 13, 2022

Regular moderate-to-vigorous physical activity (PA) and increased levels of cardiorespiratory fitness (CRF) or aerobic capacity are widely promoted as cardioprotective measures in the primary secondary prevention atherosclerotic cardiovascular (CV) disease (CVD). Nevertheless, inactivity sedentary behaviors remain a worldwide concern. The continuing coronavirus (COVID-19) pandemic has been especially devastating to patients with known occult CVD since sitting time recreational PA have reported increase decrease by 28% 33%, respectively. Herein, this first 2-part series, we discuss foundational factors exercise programming, specific reference energy metabolism, contemporary recommendations, dose-response relationship medicine, benefits regular training, including preconditioning phenotype, well CV risks PA. Finally, 'extreme hypothesis,' specifically potential maladaptations resulting from high-volume, high-intensity training programs, accelerated coronary artery calcification incident atrial fibrillation. latter is commonly depicted reverse J-shaped U-shaped curve. On other hand, longevity data argue against relationship, elite endurance athletes live 3–6 years longer than general population.

Language: Английский

Citations

60