Targeting Endoplasmic Reticulum Stress by Natural and Chemical Compounds Ameliorates Cisplatin-Induced Nephrotoxicity: A Review DOI
Habibeh Mashayekhi‐Sardoo, Ramin Rezaee, Fatemeh Yarmohammadi

et al.

Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 30, 2024

Language: Английский

A CXCR4-targeted immunomodulatory nanomedicine for photodynamic amplified immune checkpoint blockade therapy against breast cancer DOI
Yibin Liu,

Xiayun Chen,

Wei Zhang

et al.

Acta Biomaterialia, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0

Exploring Stressors: Impact on Cellular Organelles and Implications for Cellular Functions DOI Creative Commons
Zoofa Zayani, Arash Matinahmadi, Alireza Tavakolpournegari

et al.

Stresses, Journal Year: 2025, Volume and Issue: 5(2), P. 26 - 26

Published: April 4, 2025

Cellular stressors have been demonstrated to exert a substantial influence on the functionality of organelles, thereby impacting cellular homeostasis and contributing development disease pathogenesis. This review aims examine impact diverse stressors, including environmental, chemical, biological, physical factors, critical organelles such as cell membrane, mitochondria, endoplasmic reticulum, Golgi apparatus, lysosomes, membrane-less organelles. The intricate molecular mechanisms underlying stress responses, encompassing oxidative stress, protein misfolding, metabolic reprogramming, capacity elicit adaptive responses or culminate in pathological conditions. interplay between these organelle dysfunction has implicated myriad diseases, neurodegenerative disorders, cancer, immune-related pathologies. A comprehensive understanding by which respond can offer valuable insights into therapeutic strategies aimed at mitigating damage.

Language: Английский

Citations

0

Mitochondrial quality control and stress signaling pathways in the pathophysiology of cardio-renal diseases DOI Creative Commons
Isabel Amador‐Martínez, Ana Karina Aranda‐Rivera,

Mauricio Raziel Martínez-Castañeda

et al.

Mitochondrion, Journal Year: 2025, Volume and Issue: unknown, P. 102040 - 102040

Published: April 1, 2025

Mitochondria are essential organelles for cellular function and have become a broad field of study. In cardio-renal diseases, it has been established that mitochondrial dysfunction is primary mechanism leading to these pathologies. Under stress, mitochondria can develop stress response mechanisms maintain quality control (MQC) functions. contrast, the perturbation associated with pathogenesis several diseases. Thus, targeting specific pathways within MQC could offer therapeutic avenue protecting integrity. However, related signaling in axis poorly explored. The limitations include lack reproducibility experimental models disease, incomplete knowledge molecules generate bidirectional damage, temporality study models. Therefore, we believe integration all those limitations, along recent advances (i.e., mitophagy), (e.g., integrated response, unfolded protein import), pharmacology, targeted approaches reveal what deregulation like provide ideas generating strategies seek avoid progression

Language: Английский

Citations

0

Endurance Training Alleviates Metabolic-associated Fatty-liver Disease (MAFLD)-related Testicular Impairments via ER Stress Regulation DOI
Vahid Kazemizadeh,

Nastaran Teimouri,

Azita Faramarzi

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 18, 2025

Abstract Metabolic-associated fatty liver disease (MAFLD), the most prevalent disorder globally, affects 20–40% of population and presents significant health challenges. Studies link MAFLD to male reproductive dysfunction, highlighting need for effective interventions. This study investigates impact on testicular function evaluates protective role endurance training, with a focus PERK-EIF2α-ATF4 signaling pathway. Forty-four rats were allocated into two dietary groups (n = 22 each): standard diet control group (C) high-fat supplemented fructose water (FL). After 17 weeks, histological analysis confirmed development in FL group, while showed no pathological changes. Each was further subdivided sedentary endurance-trained (T) subgroups 10 per subgroup), resulting four experimental groups: C, C + T, FL. At end research, thyroid hormones (T3, T4, TSH), sex (testosterone, LH, FSH) as well PERK, EIF2α AFT4 expression assessed. Our result indicated that led weight gain, disrupted serum levels hormones, impaired hormone profiles. Additionally, triggered ER stress, evidenced by dysregulated genes Remarkably, training mitigated these adverse effects normalizing hormonal profiles restoring stress-related genes. These findings highlight critical stress MAFLD-induced dysfunction.

Language: Английский

Citations

0

Endurance Training Alleviates Metabolic‐Associated Fatty‐Liver Disease (MAFLD)‐Related Testicular Impairments via Endoplasmic Reticulum Stress Regulation DOI Creative Commons

Nastaran Teimouri,

Vahid Kazemizadeh

Journal of Clinical Laboratory Analysis, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

ABSTRACT Background Metabolic‐associated fatty liver disease (MAFLD), the most prevalent disorder globally, affects 20%–40% of population and presents significant health challenges. Studies link MAFLD to male reproductive dysfunction, highlighting need for effective interventions. This study investigates impact on testicular function evaluates protective role endurance training, with a focus GRP78‐IRE‐1α‐ATF6 signaling pathway. Methods Forty‐four rats were allocated into two dietary groups ( n = 22 each): standard diet control group (C) high‐fat supplemented fructose water (FL). After 17 weeks, histological analysis confirmed development in FL group, while showed no pathological changes. Each was further subdivided sedentary endurance‐trained (T) subgroups 10 per subgroup), resulting four experimental groups: C, C + T, FL. At end research, thyroid stimulating hormone (TSH), sex hormones (testosterone), tumor necrosis factor‐alpha (TNF‐a) as well GRP78, IRE‐1α, AFT6 expression assessed. Results Our results indicated that led weight gain, disrupted serum levels thyroid‐stimulating hormone, impaired profile. Additionally, triggered ER stress, evidenced by dysregulated genes Remarkably, training mitigated these adverse effects normalizing hormonal profiles restoring stress‐related genes. These findings highlight critical stress MAFLD‐induced dysfunction. Conclusion Overall, present suggests promising treatment strategy addressing its associated complications.

Language: Английский

Citations

0

Nephroprotective effects of hesperidin on ifosfamide-induced acute nephrotoxicity in rats: Role of NF-κB/TNF-α/ IL-1β, p53/caspase-3/Bax/Bcl-2, and ATF6/IRE1/PERK/GRP78 signaling pathways DOI
Özge Kandemir, Nurhan Akaras, Hasan Şimşek

et al.

Archives of Biochemistry and Biophysics, Journal Year: 2025, Volume and Issue: unknown, P. 110465 - 110465

Published: May 1, 2025

Language: Английский

Citations

0

Cadmium induces autophagy via IRE1 signaling pathway activated by Ca2+ in GC-2spd cells DOI

Yue Han,

Juan Dai,

Jinxin Cheng

et al.

Reproductive Toxicology, Journal Year: 2025, Volume and Issue: 135, P. 108950 - 108950

Published: May 19, 2025

Language: Английский

Citations

0

Oxidative Stress and Chronic Myeloid Leukemia: A Balance between ROS-Mediated Pro- and Anti-Apoptotic Effects of Tyrosine Kinase Inhibitors DOI Creative Commons
Alessandro Allegra,

Giuseppe Mirabile,

Santino Caserta

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(4), P. 461 - 461

Published: April 13, 2024

The balanced reciprocal translocation t (9; 22) (q34; q11) and the BCR-ABL fusion gene, which produce p210 bcr-abl protein production with high tyrosine kinase activity, are characteristics of chronic myeloid leukemia, a myeloproliferative neoplasm. This aberrant affects several signaling pathways connected to both apoptosis cell proliferation. It has been demonstrated that inhibitor treatment in leukemia acts by inducing oxidative stress and, depending on its level, can activate responsible for either or survival leukemic cells. Additionally, reactive oxygen species generation also mediate through genomic activation. Furthermore, it was shown role BCR-ABL-independent BCR-ABL-dependent resistance kinases, while patients were found have significantly reduced antioxidant level. ideal environment therapy is produced favorable status. We discuss latest studies aim manipulate redox system alter cancerous

Language: Английский

Citations

3

Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases DOI Creative Commons
Chenguang Ma, Yang Liu, Zhiling Fu

et al.

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

Published: July 25, 2024

The average lifespan of humans has been increasing, resulting in a rapidly rising percentage older individuals and high morbidity aging-associated diseases, especially cardiovascular diseases (CVDs). Diverse intracellular extracellular factors that interrupt homeostatic functions the endoplasmic reticulum (ER) induce ER stress. Cells employ dynamic signaling pathway unfolded protein response (UPR) to buffer Recent studies have demonstrated stress triggers various cellular processes associated with aging many including CVDs. Autophagy is conserved process involving lysosomal degradation recycling cytoplasmic components, proteins, organelles, pathogens invade cytoplasm. vital for combating adverse influence on heart. present report summarizes recent mechanism autophagy their overlap CVD pathogenesis context aging. It also discusses possible therapeutic interventions targeting might delay prevent or treat

Language: Английский

Citations

3

Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols DOI Open Access
Federica Conti,

JACKSON MCCUE,

Paul DiTuro

et al.

Nutrients, Journal Year: 2024, Volume and Issue: 16(15), P. 2430 - 2430

Published: July 26, 2024

Traumatic brain injuries (TBIs) constitute a significant public health issue and major source of disability death in the United States worldwide. TBIs are strongly associated with high morbidity mortality rates, resulting host negative outcomes long-term complications placing heavy financial burden on healthcare systems. One promising avenue for prevention treatment is design TBI-specific supplementation dietary protocols centred around nutraceuticals biochemical compounds whose mechanisms action have been shown to interfere with, potentially alleviate, some neurophysiological processes triggered by TBI. For example, evidence suggests that creatine monohydrate omega-3 fatty acids (DHA EPA) help decrease inflammation, reduce neural damage maintain adequate energy supply following injury. Similarly, melatonin may improve sleep disturbances often experienced post-TBI. The scope this narrative review summarise available literature neuroprotective effects selected nutrients context TBI-related provide an evidence-based overview be considered individuals affected by—or at risk for—concussion more severe head traumas. Prophylactic and/or therapeutic under investigation include monohydrate, acids, BCAAs, riboflavin, choline, magnesium, berry anthocyanins, Boswellia serrata, enzogenol, N-Acetylcysteine melatonin. Results from analysis also placed assessing addressing important health-related physiological parameters peri-impact period such as premorbid nutrient metabolic status, blood glucose regulation thermoregulation injury, caffeine consumption behaviours. As clinical research field rapidly emerging, comprehensive approach including appropriate nutritional interventions has potential mitigate physical, neurological, emotional inflicted TBIs, promote timely effective recovery, inform policymakers development strategies.

Language: Английский

Citations

3