Enhanced lipid metabolism reprogramming in CHF rats through IL-6-mediated cardiac glial cell modulation by digilanid C and electroacupuncture stimulation combination DOI Creative Commons
Yun Liu, Xiao Sun,

Mingqian Yuan

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Sept. 3, 2024

Background Cardiac lipid metabolism reprogramming is recognized as a critical pathological factor in the progression of chronic heart failure (CHF). The therapeutic potential digilanid C and electroacupuncture stimulation (ES) enhancing cardiac function has been established. However, optimal synergistic regulatory strategies these interventions on have yet to be elucidated. Methods This study aimed comprehensively evaluate impact C-ES combination steatosis remodeling CHF. Assessments were conducted across various dimensions, including myocardial oxygen consumption, mitochondrial function, metabolism. Additionally, we sought uncover underlying neuromolecular mechanisms. Results Our findings, at both molecular morphological levels, indicated that application ES significantly inhibited fibrosis steatosis. therapy facilitated repair neuro-vascular uncoupling induced Notably, ameliorated cardiomyocyte apoptosis enhanced biogenesis CHF, leading restructured energy supply pattern. immunofluorescence analyses revealed aggregation glial cells (CGCs) sites abnormal neurovascular coupling, response degeneration. was accompanied by marked reduction abnormally elevated expression interleukin 6 (IL-6) glutamatergic signaling, which correlated with severity aberrant activation CGCs. combined found activate Janus kinase 1 (JAK1)/signal transducer activator transcription 3 (STAT3) pathway, effectively attenuated accumulation over-recruitment CGCs deprivation nerves. Conclusion These findings underscore novel approach modulate complex interplay between dynamics metabolic dysregulation

Language: Английский

Restoring Mitochondrial Function and Muscle Satellite Cell Signaling: Remedies against Age-Related Sarcopenia DOI Creative Commons
Emanuele Marzetti, Biliana Lozanoska‐Ochser, Riccardo Calvani

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(4), P. 415 - 415

Published: March 28, 2024

Sarcopenia has a complex pathophysiology that encompasses metabolic dysregulation and muscle ultrastructural changes. Among the drivers of intracellular changes fibers in sarcopenia, mitochondria their quality control pathways play relevant roles. Mononucleated stem cells/satellite cells (MSCs) have been attributed critical role repair after an injury. The involvement supporting MSC-directed is unclear. There evidence reduction mitochondrial biogenesis blunts repair, thus indicating delivery functional to injured muscles can be harnessed limit fibrosis enhance restoration function. Injection autologous respiration-competent from uninjured sites damaged tissue shown reduce infarct size cell survival preclinical models ischemia-reperfusion. Furthermore, incorporation donor into MSCs enhances lung cardiac repair. This strategy also tested for regeneration purposes traumatic injuries. Indeed, systemic promotes restores mass function while reducing during recovery In this review, we discuss contribution altered MSC sarcopenia illustrate prospect harnessing as therapeutic against age-related sarcopenia.

Language: Английский

Citations

11
Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis DOI Creative Commons
Fan Chen, Kedong Xu,

Yimin Han

et al.

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

Published: Dec. 24, 2024

Acute pancreatitis (AP) is an inflammatory disease of the pancreas and a complex process involving multiple factors, with mitochondrial damage playing crucial role. Mitochondrial dysfunction now considered key driver in development AP. This often presents as increased oxidative stress, altered membrane potential permeability, DNA mutations. Under stress conditions, dynamics ROS production increase, leading to decreased potential, imbalanced calcium homeostasis, activation permeability transition pore. The release (mtDNA), recognized damage-associated molecular patterns, can activate cGAS-STING1 NF-κB pathway induce pro-inflammatory factor expression. Additionally, mtDNA inflammasomes, interleukin subsequent tissue inflammation. review summarizes relationship between mitochondria AP explores protective strategies diagnosis treatment this disease. Future research on acute benefit from exploring promising avenues such antioxidants, inhibitors, new therapies that target dysfunction.

Language: Английский

Citations

2
Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment DOI Creative Commons
Qin Wang, Xin Wang,

Zhizhong Shang

et al.

Stem Cell Research & Therapy, Journal Year: 2024, Volume and Issue: 15(1)

Published: Nov. 28, 2024

Spinal cord injury (SCI) involves a continuous and dynamic cascade of complex reactions, with mitochondrial damage dysfunction-induced energy metabolism disorders playing central role throughout the process. These not only determine severity secondary injuries but also influence potential for axonal regeneration. Given critical disturbances in pathology SCI, strategies such as enhancing transport within axons to alleviate local deficits, or transplanting autologous allogeneic mitochondria restore supply damaged tissues, have emerged approaches SCI repair. aim modulate inflammatory responses apoptosis. Preclinical studies initially demonstrated that transplantation (MT) significantly reduces neuronal death promotes regeneration following spinal injury. MT achieves this by regulating signaling pathways MAPK/ERK PI3K/Akt, promoting expression growth-associated protein-43 (GAP-43) neurons, inhibiting apoptosis-related proteins like Grp78, Chop, P-Akt, thereby survival neurons. Additionally, plays vascular endothelial growth factor, facilitating tissue repair, reducing secretion pro-inflammatory cytokines TNF-α, IL-1β, IL-6. Furthermore, modulates apoptosis decreasing p-JNK, member MAPK family. In summary, reviewing detailed mechanisms underlying pathological processes we emphasize changes endogenous post-SCI exogenous This review aims provide insights basis developing more effective clinical treatments SCI.

Language: Английский

Citations

1
Mitochondrial transplantation reconstructs the oxidative microenvironment within fibroblasts to reverse photoaging DOI

Zihan Lu,

Wenhui Zhang,

Simo Wu

et al.

Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 745, P. 151214 - 151214

Published: Dec. 19, 2024

Language: Английский

Citations

1
Enhanced lipid metabolism reprogramming in CHF rats through IL-6-mediated cardiac glial cell modulation by digilanid C and electroacupuncture stimulation combination DOI Creative Commons
Yun Liu, Xiao Sun,

Mingqian Yuan

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Sept. 3, 2024

Background Cardiac lipid metabolism reprogramming is recognized as a critical pathological factor in the progression of chronic heart failure (CHF). The therapeutic potential digilanid C and electroacupuncture stimulation (ES) enhancing cardiac function has been established. However, optimal synergistic regulatory strategies these interventions on have yet to be elucidated. Methods This study aimed comprehensively evaluate impact C-ES combination steatosis remodeling CHF. Assessments were conducted across various dimensions, including myocardial oxygen consumption, mitochondrial function, metabolism. Additionally, we sought uncover underlying neuromolecular mechanisms. Results Our findings, at both molecular morphological levels, indicated that application ES significantly inhibited fibrosis steatosis. therapy facilitated repair neuro-vascular uncoupling induced Notably, ameliorated cardiomyocyte apoptosis enhanced biogenesis CHF, leading restructured energy supply pattern. immunofluorescence analyses revealed aggregation glial cells (CGCs) sites abnormal neurovascular coupling, response degeneration. was accompanied by marked reduction abnormally elevated expression interleukin 6 (IL-6) glutamatergic signaling, which correlated with severity aberrant activation CGCs. combined found activate Janus kinase 1 (JAK1)/signal transducer activator transcription 3 (STAT3) pathway, effectively attenuated accumulation over-recruitment CGCs deprivation nerves. Conclusion These findings underscore novel approach modulate complex interplay between dynamics metabolic dysregulation

Language: Английский

Citations

0