Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health DOI Creative Commons
Ne N. Wu, Haili Tian, Peijie Chen

et al.

Cells, Journal Year: 2019, Volume and Issue: 8(11), P. 1436 - 1436

Published: Nov. 14, 2019

Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. may positively affect risk factors including body weight, blood pressure, insulin sensitivity, lipid glucose metabolism, heart function, endothelial fat composition. With ever-rising prevalence obesity other types metabolic as well sedentary lifestyle, regular moderate intensity has been indicated to benefit health reduce overall disease mortality. Exercise offers a wide cadre favorable responses system such improved dynamics system, reduced coronary diseases cardiomyopathies, enhanced cardiac reserve capacity, autonomic regulation. Ample clinical experimental evidence an emerging role autophagy, conservative catabolism process degrade recycle cellular organelles nutrients, training-offered benefits. Regular physical unique form physiological stress capable triggering adaptation while autophagy selective seems be permissive adaptation. Here this mini-review, we will summarize mitochondrial namely mitophagy versus on function.

Language: Английский

Autophagy in ovary and polycystic ovary syndrome: role, dispute and future perspective DOI Open Access

Sanjana Kumariya,

Vaibhave Ubba,

Rajesh Kumar Jha

et al.

Autophagy, Journal Year: 2021, Volume and Issue: 17(10), P. 2706 - 2733

Published: June 23, 2021

Polycystic ovary syndrome (PCOS) is a unification of endocrine and metabolic disorders has become immensely prevalent among women fertile age. The prime organ affected in PCOS the its distressed functioning elicits disturbed reproductive outcomes. In ovary, macroautophagy/autophagy performs pivotal role directing chain events starting from oocytes origin until fertilization. Recent discoveries demonstrate significant autophagy pathogenesis PCOS. Defective follicular cells during different stages follicles observed ovary. Exploring pathways provides platform for predicting possible cause altered ovarian physiology this review, we have emphasized autophagy’s governing development under normal circumstances PCOS, including abnormalities associated with such as anovulation, hyperandrogenemia, disturbances, related abnormality. So far, few studies linked propose essential progression. However, detailed knowledge area lacking. Here summarized latest to This review’s main objective provide background connection suggested novel proposal future aid better understanding pathogenesis.Abbreviations: AE: androgen excess; AF: antral follicle; AKT/PKB: AKT serine/threonine kinase; AMH: anti-Mullerian hormone; AMPK: AMP-activated protein ATG: autophagy-related; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; BMP: bone morphogenetic protein; CASP3: caspase 3; CL: corpus luteum; CYP17A1/P450C17: cytochrome P450 family 17 subfamily A member CYP19A1: 19 DHEA: dehydroepiandrosterone; EH: endometrial hyperplasia; FF: fluid; FOXO: forkhead box O; FSH: follicle stimulating GC: granulosa cell; GDF: growth differentiation factor; HA: hyperandrogenemia; HMGB1: high mobility group IGF1: insulin like factor INS: insulin; IR: resistance; LHCGR/LHR: luteinizing hormone/choriogonadotropin receptor; MAP1LC3B/LC3B: microtubule 1 light 3 beta; MAPK/ERK: mitogen-activated MAPK8/JNK: kinase 8; MTOR: mechanistic target rapamycin MTORC: complex; NAFLD: nonalcoholic fatty liver disease; NFKB: nuclear kappa B; OLR1/LOX-1: oxidized low density lipoprotein receptor oxLDL: low-density lipoproteins; PA: palmitic acid; PCOS: polycystic syndrome; PF: primary PGC: primordial germ PI3K: phosphoinositide 3-kinase; PMF: ROS: reactive oxygen species; RP: resting pool; SIRT1: sirtuin SQSTM1/p62: sequestosome T2DM: type 2 diabetes mellitus; TC: theca TUG1: taurine up-regulated

Language: Английский

Citations

186
Increased Drp1 Acetylation by Lipid Overload Induces Cardiomyocyte Death and Heart Dysfunction DOI Open Access
Qingxun Hu, Huiliang Zhang,

Nicolás Gutiérrez Cortés

et al.

Circulation Research, Journal Year: 2020, Volume and Issue: 126(4), P. 456 - 470

Published: Jan. 3, 2020

Lipid overload-induced heart dysfunction is characterized by cardiomyocyte death, myocardial remodeling, and compromised contractility, but the impact of excessive lipid supply on cardiac function remains poorly understood.To investigate regulation mitochondrial fission protein Drp1 (dynamin-related 1) in death dysfunction.Mice fed a high-fat diet (HFD) developed signs obesity type II diabetes mellitus, including hyperlipidemia, hyperglycemia, hyperinsulinemia, hypertension. HFD for 18 weeks also induced hypertrophy, fibrosis, insulin resistance, death. stimulated mouse hearts. Furthermore, increased level, phosphorylation (at activating serine 616 sites), oligomerization, translocation, GTPase activity hearts, indicating that was activated. Monkeys high fat cholesterol 2.5 years exhibited damage activation heart. Interestingly, decreased nicotinamide adenine dinucleotide (oxidized) levels acetylation In adult cardiomyocytes, palmitate acetylation, phosphorylation, levels, these increases were abolished restoration level. Proteomics analysis vitro screening revealed at lysine 642 (K642) hearts incubation cardiomyocytes. The nonacetylated mutation (K642R) attenuated palmitate-induced activation, its interaction with voltage-dependent anion channel 1, fission, contractile dysfunction, death.These findings uncover novel mechanism contributes to hypertrophy dysfunction. Excessive created an intracellular environment facilitated which, turn, resulting Thus, may be critical mediator as well potential target therapy.

Language: Английский

Citations

185
Autophagy in bone homeostasis and the onset of osteoporosis DOI Creative Commons
Xing Yin, Chenchen Zhou, Jingtao Li

et al.

Bone Research, Journal Year: 2019, Volume and Issue: 7(1)

Published: Oct. 2, 2019

Abstract Autophagy is an evolutionarily conserved intracellular process, in which domestic cellular components are selectively digested for the recycling of nutrients and energy. This process indispensable cell homeostasis maintenance stress responses. Both genetic functional studies have demonstrated that multiple proteins involved autophagic activities critical to survival, differentiation, functioning bone cells, including osteoblasts, osteocytes, osteoclasts. Dysregulation at level activity consequently disturbs balance between formation resorption mediates onset progression diseases, osteoporosis. review aims introduce topic autophagy, summarize understanding its relevance physiology, discuss role osteoporosis therapeutic potential.

Language: Английский

Citations

179
Obesity and ageing: Two sides of the same coin DOI
Bjorn T. Tam, José A. Morais, Sylvia Santosa

et al.

Obesity Reviews, Journal Year: 2020, Volume and Issue: 21(4)

Published: Feb. 5, 2020

Summary Conditions and comorbidities of obesity mirror those ageing age‐related diseases. Obesity share a similar spectrum phenotypes such as compromised genomic integrity, impaired mitochondrial function, accumulation intracellular macromolecules, weakened immunity, shifts in tissue body composition, enhanced systemic inflammation. Moreover, it has been shown that reduces life expectancy by 5.8 years men 7.1 women after the age 40. Shorter could be because holistically accelerates at multiple levels. Besides jeopardizing nuclear DNA modifies methylation pattern, which is associated with epigenetic different tissues. Additionally, other signs are seen individuals including telomere shortening, inflammation, functional declines. This review aims to show how “two sides same coin” through discussing predisposes an individual conditions, illness, disease. We will further demonstrate mechanisms perpetuate early‐onset chronic diseases parallel ageing.

Language: Английский

Citations

174
AMPK, a Regulator of Metabolism and Autophagy, Is Activated by Lysosomal Damage via a Novel Galectin-Directed Ubiquitin Signal Transduction System DOI Creative Commons
Jingyue Jia,

Bhawana Bissa,

Lukas Brecht

et al.

Molecular Cell, Journal Year: 2020, Volume and Issue: 77(5), P. 951 - 969.e9

Published: Jan. 28, 2020

Language: Английский

Citations

149
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

116
Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease DOI

Qiannan Ren,

Qiming Sun, Junfen Fu

et al.

Autophagy, Journal Year: 2023, Volume and Issue: 20(2), P. 221 - 241

Published: Sept. 12, 2023

Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases with a global rising prevalence, which closely associated high-fat diet (HFD) intake. Macroautophagy/autophagy an evolutionarily conserved degradation process for cytosolic macromolecules and damaged organelles. The potential role autophagy in hepatic lipid metabolism has been recognized, while dysfunction found to contribute NAFLD. Herein, we provide overview phases regulatory machinery, current understanding its protective HFD-induced We also discuss genetic pharmacological interventions that may help elucidate molecular mechanisms influence future therapeutic direction

Language: Английский

Citations

44
Inflammation in atherosclerosis: pathophysiology and mechanisms DOI Creative Commons
Amir Ajoolabady, Domenico Praticò, Ling Lin

et al.

Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(11)

Published: Nov. 11, 2024

Abstract Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of disease (CVD) such as coronary artery and heart failure. Ample clinical experimental evidence has corroborated vital inflammation pathophysiology atherosclerosis. Hence, demand for preclinical research into atherosclerotic is horizon. Indeed, acquisition an in-depth knowledge molecular cellular mechanisms atherosclerosis should allow us identify novel therapeutic targets with translational merits. In this review, we aimed critically discuss speculate recently identified Moreover, delineated various signaling cascades proinflammatory responses macrophages other leukocytes that promote plaque end, highlighted potential targets, pros cons current interventions, well anti-inflammatory atheroprotective mechanisms.

Language: Английский

Citations

24
Autophagy in aging-related diseases and cancer: Principles, regulatory mechanisms and therapeutic potential DOI
Na Wu, Wenhui Zheng,

Yundong Zhou

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 100, P. 102428 - 102428

Published: July 20, 2024

Language: Английский

Citations

22
Therapeutic potential of melatonin related to its role as an autophagy regulator: A review DOI Open Access
José Antonio Boga, Beatriz Caballero, Yaiza Potes

et al.

Journal of Pineal Research, Journal Year: 2018, Volume and Issue: 66(1)

Published: Oct. 17, 2018

There are several pathologies, syndromes, and physiological processes in which autophagy is involved. This process of self-digestion that cells trigger as a survival mechanism complex tightly regulated, according to the homeostatic conditions organ. However, all cases, its relationship with oxidative stress alterations evident, following pathway suggests endoplasmic reticulum and/or mitochondrial changes. accumulating evidence beneficial role melatonin has regulation restoration damaged autophagic processes. In this review, we focus on major changes such aging essential pathologies including cancer, neurodegenerative diseases, viral infections obesity, document each these different situations.

Language: Английский

Citations

155