Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights

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

Published: Feb. 14, 2024

Abstract Cardiovascular diseases and cancer are the leading causes of death in Western world share common risk factors. Reduced cardiorespiratory fitness (CRF) is a major determinant cardiovascular morbidity survival. In this review we discuss cancer- induced disturbances parenchymal, cellular, mitochondrial function, which limit CRF may be antagonized attenuated through exercise training. We show impact on survival its attenuating effects cardiotoxicity cancer-related treatment. Tailored programs not yet available for each tumor entity as several trials were performed heterogeneous populations without adequate cardiopulmonary testing (CPET) prior to prescription with wide variation modalities. There emerging evidence that crucial pillar treatment tool mitigate cardiotoxic effects. modalities aerobic resistance training their potential improve patients provide an example periodization model cancer.

Language: Английский

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Mitochondrial stress: a key role of neuroinflammation in stroke

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: Feb. 6, 2024

Abstract Stroke is a clinical syndrome characterized by an acute, focal neurological deficit, primarily caused the occlusion or rupture of cerebral blood vessels. In stroke, neuroinflammation emerges as pivotal event contributing to neuronal cell death. The occurrence and progression entail intricate processes, prominently featuring mitochondrial dysfunction adaptive responses. Mitochondria, double membrane-bound organelle are recognized “energy workshop” body. Brain particularly vulnerable disturbances due its high energy demands from mitochondria-related production. interplay between mitochondria plays significant role in pathogenesis stroke. biological pathological consequences resulting stress have substantial implications for function. Mitochondrial serves mechanism aimed at mitigating induced import misfolded proteins, which occurs response This involves reduction protein accumulation overall synthesis. influence on state stroke underscored capacity interact with neuroinflammation. impact varies according severity. Moderate can bolster cellular defenses, enabling cells better withstand detrimental stressors. contrast, sustained excessive detrimentally affects tissue integrity. relationship depends degree present. Understanding instrumental excavating novel treatment review aims provide evaluation cross-talk within context We aim reveal how environment

Language: Английский

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Mitochondria during T cell aging

Seminars in Immunology, Journal Year: 2023, Volume and Issue: 69, P. 101808 - 101808

Published: July 18, 2023

Mitochondrial dysfunction is a hallmark of aging that contributes to inflammaging. It characterized by alterations the mitochondrial DNA, reduced respiratory capacity, decreased membrane potential and increased reactive oxygen species production. These primary disrupt other interconnected important mitochondrial-related processes such as metabolism, dynamics biogenesis, mitophagy, calcium homeostasis or apoptosis. In this review, we gather current knowledge about different which are altered during aging, with special focus on their contribution age-associated T cell

Language: Английский

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Epilepsy: Mitochondrial connections to the ‘Sacred’ disease

Mitochondrion, Journal Year: 2023, Volume and Issue: 72, P. 84 - 101

Published: Aug. 13, 2023

Over 65 million people suffer from recurrent, unprovoked seizures. The lack of validated biomarkers specific for myriad forms epilepsy makes diagnosis challenging. Diagnosis and monitoring childhood add to the need non-invasive biomarkers, especially when evaluating antiseizure medications. Although underlying mechanisms epileptogenesis are not fully understood, evidence mitochondrial involvement is substantial. Seizures affect 35%-60% patients diagnosed with diseases. Mitochondrial dysfunction pathophysiological in various epilepsies, including those non-mitochondrial origin. Decreased ATP production caused by malfunctioning brain cell mitochondria leads altered neuronal bioenergetics, metabolism neurological complications, Iron-dependent lipid peroxidation initiates ferroptosis, a death pathway that aligns morphology found neurodegenerative diseases (NDDs). Studies mouse genetic models seizure phenotypes where function an essential selenoprotein (GPX4) targeted suggest roles ferroptosis epilepsy. GPX4 pivotal NDDs, selenium protects interneurons ferroptosis. Selenium central nervous system micronutrient trace element. Low serum concentrations other elements minerals, iron, noted diagnosing supplements alleviate intractable seizures children reduced GPX activity. Copper cuproptosis, like iron link NDDs. Connecting these mechanistic pathways selenoproteins provides new insights into treating seizures, pointing using medicines prodrugs lipoic acid treat potential alternative therapeutic approaches transcranial magnetic stimulation (transcranial), photobiomodulation vagus nerve stimulation.

Language: Английский

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Mitochondrial Stress and Mitokines: Therapeutic Perspectives for the Treatment of Metabolic Diseases

Diabetes & Metabolism Journal, Journal Year: 2024, Volume and Issue: 48(1), P. 1 - 18

Published: Jan. 4, 2024

Mitochondrial stress and the dysregulated mitochondrial unfolded protein response (UPR^mt) are linked to various diseases, including metabolic disorders, neurodegenerative cancer. Mitokines, signaling molecules released by UPR^mt, crucial mediators of inter-organ communication influence systemic physiological processes. In this review, we provide a comprehensive overview mitokines, their regulation exercise lifestyle interventions implications for diseases. The endocrine actions mitokines related adaptations highlighted, specifically broad functions fibroblast growth factor 21 differentiation 15, as well specific in regulating inter-tissue homeostasis. Finally, discuss potential genetic reduce hazards associated with mitokine preserve an equilibrium stress-induced responses. This review provides valuable insights into mechanisms underlying health disease exploring interactions regulation, which will facilitate development targeted therapies personalized improve outcomes quality life.

Language: Английский

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ATP releasing channels and the ameliorative effects of high intensity interval training on diabetic heart: a multifaceted analysis

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: March 26, 2024

Abstract Type 2 diabetes (T2D) can cause severe cardiac complications at functional, histologic and molecular levels. These pathological could be mediated by ATP-releasing channels such as Panx1 ATP receptors, in particular P2X7. The aim of our study was to investigate the effect high-intensity interval training (HIIT) on T2D-induced histopathological levels, with a focus channels. 48 male Wistar rats age 8 weeks were randomly allocated into four groups: control (Con), Diabetes (T2D), Training (TR), + (T2D TR). T2D induced high-fat diet plus low dose (35 mg/kg) STZ administration. Rats TR groups underwent an 8-weeks program involving intervals ranging from 80 100% their maximum running speed (Vmax), 4–10 per session. Protein expression Interleukin 1β (IL1β), 10 (IL-10), Pannexin 1 (Panx1), P2X7R (purinergic P2X receptor 7), NLRP1 (NLR Family Pyrin Domain Containing 1), BAX, Bcl2 measured heart tissue. Additionally, we assessed function, changes, well insulin resistance using homeostasis model assessment (HOMA-IR). In contrast group, HIIT led increased protein IL-10 heart. It also resulted improvements systolic diastolic blood pressures, rate, ± dp/dt (maximum minimum changes left ventricular pressure), while reducing IL-1β, Panx1, P2X7R, NLRP1, BAX levels Furthermore, pressure (LVDP) reduced ( P ≤ 0.05). Moreover, lesion scores but decreased HIIT, along reduction fibrosis percentage results this suggest that cardioprotective effects diabetic may modulation This lead inflammation apoptosis, improve attenuate injury fibrosis.

Language: Английский

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Small peptides: could they have a big role in metabolism and the response to exercise?

The Journal of Physiology, Journal Year: 2024, Volume and Issue: 602(4), P. 545 - 568

Published: Jan. 9, 2024

Abstract Exercise is a powerful non‐pharmacological intervention for the treatment and prevention of numerous chronic diseases. Contracting skeletal muscles provoke widespread perturbations in cells, tissues organs, which stimulate multiple integrated adaptations that ultimately contribute to many health benefits associated with regular exercise. Despite much research, molecular mechanisms driving such changes are not completely resolved. Technological advancements beginning early 1960s have opened new avenues explore responsible beneficial This has led increased research into role small peptides (<100 amino acids) mitochondrially derived metabolism disease, including those coded within open reading frames (sORFs; coding sequences encode peptides). Recently, it been hypothesized sORF‐encoded other play significant roles as exercise‐sensitive exercise‐induced physiological adaptation. In this review, we highlight discovery newly discovered involved metabolism, specific emphasis on their functions metabolic light few studies available, also present data how both single exercise sessions training affect expression peptides. Finally, outline questions await investigation regarding various diseases, addition adaptations, future studies. image

Language: Английский

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Ultrasound‑targeted microbubble destruction technology delivering β‑klotho to the heart enhances FGF21 sensitivity and attenuates heart remodeling post‑myocardial infarction

International Journal of Molecular Medicine, Journal Year: 2024, Volume and Issue: 53(6)

Published: April 24, 2024

Fibroblast growth factor (FGF)21 is a peptide hormone that improves mitochondrial function and energy metabolism, the deficiency of its co‑receptor β‑klotho (KLB) causes decreased FGF21 sensitivity. The present study examined whether cardiac delivery plasmids containing KLB gene via ultrasound‑targeted microbubble destruction (UTMD) enhances efficacy against heart failure post‑acute myocardial infarction (AMI). For this purpose, levels in patients rats with dysfunction post‑infarction were determined using ELISA. Sprague‑Dawley received 3X UTMD‑mediated KLB@cationic microbubbles (KLB@CMBs) 1 week following induction AMI. Echocardiography, histopathology biochemical analysis performed at 4 weeks results revealed had higher serum than healthy controls. However, downstream signal, KLB, but not α‑klotho, was reduced tissues As expected, treatment did substantially attenuate remodeling post‑infarction. It found receptors KLB may result insensitivity to treatment. In vivo, UTMD technology‑mediated KLB@CMBs significantly enhanced effects administration on infarction. by attenuated impairment oxidative stress activating nuclear erythroid 2‑related 2 signals. On whole, demonstrates optimizes cardioprotective therapy adverse remodeling. appears promising interdisciplinary approach which improve post‑myocardial

Language: Английский

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Exercise mitigates age-related metabolic diseases by improving mitochondrial dysfunction

Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 91, P. 102087 - 102087

Published: Oct. 11, 2023

Language: Английский

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Proteomics validate circulating GDF-15 as an independent biomarker for COVID-19 severity

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: April 15, 2024

Introduction Growth differentiation factor 15 (GDF-15) was originally described as a stress-induced cytokine, and biomarker of aging cardiovascular diseases. We hypothesized that circulating GDF-15 would be associated with COVID-19 disease severity. Herein, we explored this hypothesis in large cohort patients. Methods Blood samples were collected from 926 adult patients 285 hospitalized controls the Biobanque Québécoise de la (BQC19). severity graded according to WHO criteria. SOMAscan proteomics assay performed on 50µL plasma. ELISA 46 selected participants left-over plasma validate differences levels. Statistical analyses conducted using GraphPad Prism 9.0 SPSS. P values &lt; 0.01 considered significant. Results Proteomics showed levels higher compared controls. increased presenting comorbidities including diabetes, cancer, chronic obstructive pulmonary (COPD) had revealed significant elevation until 30 days after hospitalization. Plasma correlated older age. Moreover, pro-inflammatory cytokine interleukin-6 (IL-6) inflammation marker C-reactive protein (CRP) well soluble its putative receptor CD48. No association established between anti-SARS-CoV-2 IgG Conclusions This study confirms for Clinical evaluation could assist identification persons at high-risk progressing severe disease, thus improving patient care.

Language: Английский

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