Interplay of G-proteins and Serotonin in the Neuroimmunoinflammatory Model of Chronic Stress and Depression: A Narrative Review DOI
Evgeni Gusev, Alexey Sarapultsev

Current Pharmaceutical Design, Год журнала: 2023, Номер 30(3), С. 180 - 214

Опубликована: Дек. 28, 2023

Introduction: This narrative review addresses the clinical challenges in stress-related disorders such as depression, focusing on interplay between neuron-specific and pro-inflammatory mechanisms at cellular, cerebral, systemic levels. Objective: We aim to elucidate molecular linking chronic psychological stress with low-grade neuroinflammation key brain regions, particularly roles of G proteins serotonin (5-HT) receptors. Methods: comprehensive literature employs systematic, narrative, scoping methodologies, combined approaches general pathology. It synthesizes current research shared signaling pathways involved responses neuroinflammation, including calcium-dependent mechanisms, mitogen-activated protein kinases, transcription factors like NF-κB p53. The also focuses role protein-coupled neurotransmitter receptors (GPCRs) immune responses, a detailed analysis how 13 14 types human 5-HT contribute depression neuroinflammation. Results: reveals complex interaction signals immunoinflammatory pathologies. highlights GPCRs canonical inflammatory mediators influencing both pathological physiological processes nervous tissue. Conclusion: proposed Neuroimmunoinflammatory Stress Model (NIIS Model) suggests that proinflammatory pathways, mediated by metabotropic ionotropic receptors, are crucial for maintaining neuronal homeostasis. Chronic mental can disrupt this balance, leading increased states contributing neuropsychiatric psychosomatic disorders, depression. model integrates traditional theories pathogenesis, offering understanding multifaceted nature condition.

Язык: Английский

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

Yundong Zhou

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер 100, С. 102428 - 102428

Опубликована: Июль 20, 2024

Язык: Английский

Процитировано

19
Interplay between Cell Death and Cell Proliferation Reveals New Strategies for Cancer Therapy DOI Open Access
Luke V. Loftus, Sarah R. Amend, Kenneth J. Pienta

и другие.

International Journal of Molecular Sciences, Год журнала: 2022, Номер 23(9), С. 4723 - 4723

Опубликована: Апрель 25, 2022

Cell division and cell death are fundamental processes governing growth development across the tree of life. This relationship represents an evolutionary link between cycle programs that is present in all cells. Cancer characterized by aberrant regulation both, leading to unchecked proliferation replicative immortality. Conventional anti-cancer therapeutic strategies take advantage proliferative dependency cancer yet, doing so, triggering apoptosis, a pathway which inherently resistant. A thorough understanding how therapeutics kill cells needed develop novel, more durable treatment strategies. While evolves cell-intrinsic resistance physiological pathways, there opportunities for agnostic forms death, example, necroptosis or ferroptosis. Furthermore, independent immunogenic, potentially licensing host immunity additional antitumor activity. Identifying vulnerabilities critical developing alternative can overcome resistance.

Язык: Английский

Процитировано

64
ATM: Main Features, Signaling Pathways, and Its Diverse Roles in DNA Damage Response, Tumor Suppression, and Cancer Development DOI Open Access
Liem Phan, Abdol-Hossein Rezaeian

Genes, Год журнала: 2021, Номер 12(6), С. 845 - 845

Опубликована: Май 30, 2021

ATM is among of the most critical initiators and coordinators DNA-damage response. canonical non-canonical signaling pathways involve hundreds downstream targets that control many important cellular processes such as DNA damage repair, apoptosis, cell cycle arrest, metabolism, proliferation, oxidative sensing, others. Of note, often considered a major tumor suppressor because its ability to induce apoptosis arrest. However, in some advanced stage cells, increased confers remarkable advantages for cancer survival, resistance radiation chemotherapy, biosynthesis, metastasis. This review focuses on addressing characteristics, especially diverse roles homeostasis development.

Язык: Английский

Процитировано

62
Mitochondrial Dysfunction and Mitophagy in Type 2 Diabetes: Pathophysiology and Therapeutic Targets DOI
Nadezda Apostolova, Teresa Vezza, Jordi Muntané

и другие.

Antioxidants and Redox Signaling, Год журнала: 2023, Номер 39(4-6), С. 278 - 320

Опубликована: Янв. 15, 2023

Significance: Type 2 diabetes mellitus, which is related to oxidative stress and mitochondrial dysfunction, one of the most prevalent diseases in world. In past decade, alterations autophagy have been shown play a fundamental role development control type diabetes. Further, mitophagy has recognized as key player eliminating dysfunctional mitochondria this disease. Recent Advances: Recently, much progress made understanding molecular events associated with stress, Critical Issues: Despite increasing evidence relationship between their pathophysiolology diabetes, effective therapeutic strategies combat disease through targeting mitochondria, autophagy, are yet be implemented. Future Directions: This review provides wide perspective existing literature concerning complicated interplay mitophagy, dysfunction potential targets based on these mechanisms explored. Antioxid. Redox Signal. 39, 278-320.

Язык: Английский

Процитировано

23
Therapeutic targeting of senescent cells in the CNS DOI
Markus Rießland, Methodios Ximerakis, Andrew A. Jarjour

и другие.

Nature Reviews Drug Discovery, Год журнала: 2024, Номер unknown

Опубликована: Сен. 30, 2024

Язык: Английский

Процитировано

11
Low-Dose Non-Targeted Effects and Mitochondrial Control DOI Open Access
D. Averbeck

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(14), С. 11460 - 11460

Опубликована: Июль 14, 2023

Non-targeted effects (NTE) have been generally regarded as a low-dose ionizing radiation (IR) phenomenon. Recently, regarding long distant abscopal also observed at high doses of IR) relevant to antitumor therapy. IR is inducing NTE involving intracellular and extracellular signaling, which may lead short-ranging bystander long-ranging signaling effects. Internal “spontaneous” cellular stress mostly due metabolic oxidative mitochondrial energy production (ATP) through phosphorylation and/or anaerobic pathways accompanied by the leakage O2− other radicals from mitochondria during normal or increased requirements dysfunction. Among external stressors, has shown very rapidly perturb functions, leading supply demands ROS/NOS production. Depending on dose, this affects all types cell constituents, including DNA, RNA, amino acids, proteins, membranes, perturbing inner organization function, forcing cells reorganize metabolism network organelles. The reorganization implies cytoplasmic-nuclear shuttling important activation autophagy, mitophagy, well induction cycle arrest, DNA repair, apoptosis, senescence. It includes reprogramming genetic epigenetic control expression genes proteins in order ensure tissue survival. At low IR, directly irradiated already exert non-targeted release molecular mediators, such radicals, cytokines, fragments, small RNAs, (sometimes form vehicles exosomes), can induce damage unirradiated neighboring (abscopal) immune responses. Such are contributing phenomena, hormesis, adaptive responses, hypersensitivity, genomic instability, they promoting suppression cells. All these parts main defense systems tissues, IR-induced innate present review focused prominent role processes, determinants survival anti-tumor RT.

Язык: Английский

Процитировано

16
Emerging Insight Into the Role of Circadian Clock Gene BMAL1 in Cellular Senescence DOI Creative Commons

Wenqian Zhang,

Yuan Xiong, Ranyang Tao

и другие.

Frontiers in Endocrinology, Год журнала: 2022, Номер 13

Опубликована: Июнь 6, 2022

Cell senescence is a crucial process in cell fate determination and involved an extensive array of aging-associated diseases. General perceptions experimental evidence point out that the decline physical function as well diseases are often initiated by organ ageing. Therefore, regulation can be promising way to handle such osteoporosis. The circadian clock regulates wide range cellular physiological activities, many age-linked degenerative disorders associated with dysregulation genes. BMAL1 core transcription factor governs downstream genes binding E-box elements their promoters. Compelling has proposed role In this review, we summarize linkage between factors including oxidative stress, metabolism, genotoxic stress response. Dysregulated dampened may serve potential therapeutic target against aging-

Язык: Английский

Процитировано

24
Substrate stiffness dictates unique doxorubicin-induced senescence-associated secretory phenotypes and transcriptomic signatures in human pulmonary fibroblasts DOI
Huixun Du, Jacob Rose, Joanna Bons

и другие.

GeroScience, Год журнала: 2025, Номер unknown

Опубликована: Янв. 18, 2025

Язык: Английский

Процитировано

0
The link between Mitochondria and Sarcopenia DOI Creative Commons

Nurul Tihani Kamarulzaman,

Suzana Makpol

Journal of Physiology and Biochemistry, Год журнала: 2025, Номер unknown

Опубликована: Фев. 19, 2025

Язык: Английский

Процитировано

0
Recent Advances in Anti‐Aging Therapeutic Strategies Targeting DNA Damage Response and Senescence‐Associated Secretory Phenotype‐Linked Signaling Cascade DOI

Jawad Nadeem,

Rukhsana Sultana,

Amna Parveen

и другие.

Cell Biochemistry and Function, Год журнала: 2025, Номер 43(3)

Опубликована: Фев. 26, 2025

ABSTRACT Aging is considered the contributory accumulation of abruptions occurring through cell signaling cascades, which ultimately cause changes in physical functions, fate, and damage across all organ systems. DNA response (DDR) also occurs telomere shortening, tumor formation, mitochondrial dysfunction, so forth. Cellular aging cycle arrest, result extended DDR cascade networks via MDC1, 53BP1, H2AX, ATM, ARF, P53, P13‐Akt, BRAF, Sirtuins, NAD + , These persistent arrests initiated by other associated stress‐induced signals promote a permanent state arrest called senescence‐associated secretory phenotype (SASP). However, cellular gets accelerated with faulty repair systems, produced senescent cells further generate various promoting contributors to age‐related dysfunctional diseases including SASP. Any these factors contribute disease development. Therefore, this review explores anti‐aging targeting SASP regulation their detailed networks. In addition, it allows researchers identify targets therapeutic strategies based on identified nonidentified targets.

Язык: Английский

Процитировано

0