Kidney International Reports, Год журнала: 2024, Номер unknown
Опубликована: Дек. 1, 2024
Язык: Английский
Cancers, Год журнала: 2024, Номер 16(12), С. 2262 - 2262
Опубликована: Июнь 18, 2024
Melanoma, originating through malignant transformation of melanin-producing melanocytes, is a formidable malignancy, characterized by local invasiveness, recurrence, early metastasis, resistance to therapy, and high mortality rate. This review discusses etiologic risk factors for melanoma, diagnostic prognostic tools, including recent advances in molecular biology, omics, bioinformatics, provides an overview its therapy. Since the incidence melanoma rising remains unacceptably high, we discuss inherent properties, melanogenesis, that make this disease resilient treatment propose use AI solve above complex multidimensional problems. We provide on vitamin D anticancerogenic report field can solutions prevention and/or therapy melanoma. Experimental papers clinicopathological studies role status signaling pathways initiated active metabolites prognosis are reviewed. conclude signaling, defined specific nuclear receptors selective activation hydroxyderivatives, benefit new or existing therapeutic approaches. target with computational biology tools solution problem.
Язык: Английский
Процитировано
22
Redox Biology, Год журнала: 2025, Номер unknown, С. 103518 - 103518
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
2
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(7), С. 3367 - 3367
Опубликована: Апрель 3, 2025
Parkinson's disease (PD), a prevalent neurodegenerative disorder, demonstrates the critical involvement of endoplasmic reticulum stress (ERS) in its pathogenesis. This review comprehensively examines role and molecular mechanisms ERS PD. represents cellular response triggered by imbalances (ER) homeostasis, induced factors such as hypoxia misfolded protein aggregation, which activate unfolded (UPR) through inositol-requiring enzyme 1 (IRE1), kinase R-like (PERK), activating transcription factor 6 (ATF6) pathways. Clinical, animal model, studies have consistently demonstrated strong association between PD ERS. Abnormal expression ERS-related molecules patients' brains cerebrospinal fluid (CSF) correlates with progression. In models (e.g., Drosophila mice), inhibition alleviates dopaminergic neuronal damage. Cellular experiments reveal that PD-mimicking pathological conditions induce ERS, while interactions mitochondrial dysfunction promote apoptosis. Mechanistically, (1) aggregation α-synuclein (α-syn) mutually reinforce neuron damage; (2) leucine-rich repeat 2 (LRRK2) gene mutations thrombospondin-1 (THBS1)/transforming growth beta (TGF-β1) interactions; (3) Parkin PTEN-induced (PINK1) regulate Furthermore, interacts dysfunction, oxidative stress, neuroinflammation to exacerbate injury. Emerging therapeutic strategies show significant potential, including artificial intelligence (AI)-assisted drug design targeting pathways precision medicine approaches exploring non-pharmacological interventions personalized electroacupuncture. Future research should focus on elucidating identifying novel targets develop more effective treatments for patients, ultimately improving their quality life.
Язык: Английский
Процитировано
1
Frontiers in Cell and Developmental Biology, Год журнала: 2024, Номер 12
Опубликована: Окт. 9, 2024
This article reviews the latest research progress on role of mitochondrial autophagy receptor FUN14 domain containing 1 (FUNDC1) in events and kidney disease. FUNDC1 is a protein located outer membrane mitochondria, which maintains function quality mitochondria by regulating autophagy, that is, selective degradation process mitochondria. The structural characteristics enable it to respond intracellular signal changes regulate activity through phosphorylation dephosphorylation. During phosphorylation, unc-51-like kinase (ULK1) promotes activation mitophagy phosphorylating Ser17 FUNDC1. In contrast, Src CK2 kinases inhibit interaction between LC3 Tyr18 Ser13, thereby inhibiting mitophagy. dephosphorylation, PGAM5 phosphatase enhances dephosphorylating activating BCL2L1 inhibits interacting with PGAM5, preventing dephosphorylation plays an important events, participating fission, maintaining homeostasis iron proteins matrix, mediating crosstalk endoplasmic reticulum lysosomes, have effects cell energy metabolism programmed death. aspect disease, abnormal closely related occurrence development many diseases. acute injury (AKI), cardiorenal syndrome (CRS), diabetic nephropathy (DN), chronic disease (CKD) ,renal fibrosis (RF) renal anemia, FUNDC1-mediated imbalance may be one key factors progression. Therefore, in-depth study regulatory mechanism great significance for understanding pathogenesis developing new treatment strategies.
Язык: Английский
Процитировано
5
World Journal of Diabetes, Год журнала: 2025, Номер 16(4)
Опубликована: Фев. 28, 2025
Diabetic nephropathy (DN) is a well-known microvascular complication in patients with diabetes mellitus, which characterized by the accumulation of extracellular matrix glomerular and tubulointerstitial compartments, along hyalinization intrarenal vasculature. DN has recently emerged as leading cause chronic end-stage renal disease. While pathobiology other diabetic complications, such retinopathy, largely understood reasonable therapeutic options, mechanisms management strategies for remain incompletely elucidated. In this editorial, we comment on article Liu et al, focusing underlying detrimental impact β-arrestin-2 kidneys context DN. The authors suggest that inhibiting could alleviate damage through suppressing apoptosis endothelial cells (GENCs), highlighting promising target study proposed triggers endoplasmic reticulum (ER) stress via ATF6 signaling pathway, thereby promoting GENC exacerbating progression. Given novel crucial role ER stress-related DN, it imperative to further explore β-arrestin-2, its roles potential implications
Язык: Английский
Процитировано
0
Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)
Опубликована: Март 4, 2025
Microvascular complications of diabetes pose a significant threat to global health, mainly including diabetic kidney disease (DKD), retinopathy (DR), peripheral neuropathy (DPN), and cardiomyopathy (DCM), which can ultimately lead failure, blindness, disability, heart failure. With the increasing prevalence diabetes, search for new therapeutic targets microvascular is imminent. Mitophagy widespread strictly maintained process self-renewal energy metabolism that plays an important role in reducing inflammatory responses, inhibiting reactive oxygen species accumulation, maintaining cellular metabolism. Hyperglycemia results impaired mitophagy, leads mitochondrial dysfunction exacerbates progression. This article summarizes relevant molecular mechanisms mitophagy reviews current status research on regulating as potential treatment complications, attempting give angles complications.
Язык: Английский
Процитировано
0
Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 294, С. 118062 - 118062
Опубликована: Март 23, 2025
Язык: Английский
Процитировано
0
Engineering Reports, Год журнала: 2025, Номер 7(4)
Опубликована: Апрель 1, 2025
ABSTRACT Renal ischemia–reperfusion injury (IRI) is a leading etiology of acute kidney (AKI), predominantly observed in complex cardiovascular surgeries, severe traumatic shock, and renal transplantation. Oxidative stress, calcium overload, mitochondrial dysfunction, autophagy, apoptosis are closely associated with IRI. Mitochondria not only serve as critical organelles for cellular oxidative respiration energy production but also play vital roles various biochemical processes including homeostasis, signal transduction, metabolism, cell differentiation, apoptosis, ischemia, reinjury. One particular form mitophagy, can accurately eliminate damaged or defective mitochondria, thereby maintaining homeostasis playing key role To give new approach to mechanistic research clinical prevention therapy injury, this paper examines the signaling pathways novel therapeutic targets mitophagy injury.
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(8), С. 3550 - 3550
Опубликована: Апрель 10, 2025
This study systematically elucidates the regulatory mechanisms and potential therapeutic value of exercise-induced hormone Irisin in pathological progression cardiac fibrosis. Through comprehensive analysis multidimensional data integration, we constructed a complete network within cardiovascular system, spanning its secretion, signal transduction, precise control. Our findings demonstrate that exercise intervention significantly elevates circulating levels via skeletal muscle-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-fibronectin type III domain-containing protein 5 (FNDC5) signaling axis. establishes molecular barrier against fibrosis by targeting Sirtuin 1 (Sirt1) activation, inhibiting transforming growth factor-beta (TGF-β)/Smad3 pathway, modulating transcriptional activity mitochondrial biogenesis core factors PGC-1α nuclear respiratory factor (NRF-1). Moreover, dual mechanism exercise-skeletal muscle-heart axis not only effectively suppresses aberrant activation fibroblasts but also reduces collagen deposition, oxidative stress, inflammatory infiltration restoring dynamics balance. Taken together, this reveals novel exercise-mediated cardioprotective at interaction level, thereby providing theoretical basis for development non-pharmacological bio-intervention strategies pathway laying translational foundation prescriptions diseases.
Язык: Английский
Процитировано
0
Stem Cell Research & Therapy, Год журнала: 2025, Номер 16(1)
Опубликована: Май 1, 2025
Intervertebral disc degeneration is a multifactorial degenerative disease that poses significant threat to the health of elderly population. Current treatments primarily focus on physical therapy, medication, and surgery alleviate symptoms associated with compression but do not address progression degeneration. Therefore, this review aimed explore potential extracellular vesicle therapy as novel preventive strategy delay enhance tissue repair in intervertebral discs. We cover pathogenic mechanisms underlying degeneration, including inflammation, apoptosis, pyroptosis, ferroptosis, autophagy dysregulation, roles non-coding RNAs. Subsequently, we discussed therapeutic vesicles their molecular components, such proteins, RNAs, lipids, modulating these pathways counter provides comprehensive role cargo mediating mechanisms. It discusses functional enhancement advantages exhibited by under current bioengineering modifications drug loading. The challenges future prospects utilizing treat condition are also summarized.
Язык: Английский
Процитировано
0