Mitochondria, pattern recognition receptors and autophagy under physiological and pathological conditions, including viral infections

Niedźwiedzka-Rystwej, Paulina; Bębnowska, Dominika; Kołacz, R.; Deptuła, Wiesław

doi:10.18388/abp.2020_5807

Cited by 2 publications

(2 citation statements)

References 61 publications

(178 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We identified and screened four mitochondrial hub genes ( AMPK , PGC1-α , SLC25A25 , and ARMCX1 ). Recent studies have found that inflammation is usually activated by PRRs on both immune and non-immune cells [ 24 ]. Notably, nucleic acids, proteins, and small metabolites do not normally drive the PRR signalling pathway, because they do not go to the PRRs’ subcellular compartments [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness

Li,

Peng,

Sun

et al. 2023

BMC Med Genomics

View full text Add to dashboard Cite

Background Delayed onset muscle soreness (DOMS) is a self-healing muscle pain disorder. Inflammatory pain is the main feature of DOMS. More and more researchers have realized that changes in mitochondrial morphology are related to pain. However, the role of mitochondria in the pathogenesis of DOMS and the abnormal immune microenvironment is still unknown. Methods Mitochondria-related genes and gene expression data were obtained from MitoCarta3.0 and NCBI GEO databases. The network of mitochondrial function and the immune microenvironment of DOMS was constructed by computer algorithm. Subsequently, the skeletal muscle of DOMS rats was subjected to qPCR to verify the bioinformatics results. DOMS and non-DOMS histological samples were further studied by staining and transmission electron microscopy. Results Bioinformatics results showed that expression of mitochondria-related genes was changed in DOMS. The results of qPCR showed that four hub genes (AMPK, PGC1-α, SLC25A25, and ARMCX1) were differentially expressed in DOMS. These hub genes are related to the degree of skeletal muscle immune cell infiltration, mitochondrial respiratory chain complex, DAMPs, the TCA cycle, and mitochondrial metabolism. Bayesian network inference showed that IL-6 and PGC1-α may be the main regulatory genes of mitochondrial damage in DOMS. Transmission electron microscopy revealed swelling of skeletal muscle mitochondria and disorganization of myofilaments. Conclusions Our study found that skeletal muscle mitochondrial damage is one of the causes of inflammatory factor accumulation in DOMS. According to the screened-out hub genes, this study provides a reference for follow-up clinical application.

show abstract

Section: Discussionmentioning

confidence: 99%

A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness

Li,

Peng,

Sun

et al. 2023

BMC Med Genomics

View full text Add to dashboard Cite

show abstract

“…Therefore, a wide range of strategies have been developed to induce mitochondrial apoptosis in cancer cells. 12 , 13 Mitochondrial dysfunction can lead to cell death due to ATP deficiency, prompting the proposal of various strategies for stimulating mitochondrial apoptosis in cancer therapy. The antitumor effects of Ca 2+ have led to increased attention on mitochondrial Ca 2+ overload as a promising pathway for inducing mitochondrial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Layer-by-Layer Nanoparticles for Calcium Overload in situ Enhanced Reactive Oxygen Oncotherapy

Zhang,

Man,

Guo

et al. 2024

IJN

View full text Add to dashboard Cite

Background Challenges such as poor drug selectivity, non-target reactivity, and the development of drug resistance continue to pose significant obstacles in the clinical application of cancer therapeutic drugs. To overcome the limitations of drug resistance in chemotherapy, a viable treatment strategy involves designing multifunctional nano-platforms that exploit the unique physicochemical properties of tumor microenvironment (TME). Methods Herein, layer-by-layer nanoparticles with polyporous CuS as delivery vehicles, loaded with a sonosensitizer (tetra-(4-aminophenyl) porphyrin, TAPP) and sequentially functionalized with pH‐responsive CaCO 3 , targeting group hyaluronic acid (HA) were designed and synthesized for synergistic treatment involving chemodynamic therapy (CDT), sonodynamic therapy (SDT), photothermal therapy (PTT), and calcium overload. Upon cleavage in an acidic environment, CaCO 3 nanoparticles released TAPP and Ca 2+ , with TAPP generating 1 O 2 under ultrasound trigger. Exposed CuS produced highly cytotoxic ·OH in response to H 2 O 2 and also exhibited a strong PTT effect. Results CuS@TAPP-CaCO 3 /HA (CTCH) delivered an enhanced ability to release more Ca 2+ under acidic conditions with a pH value of 6.5, which in situ causes damage to HeLa mitochondria. In vitro and in vivo experiments both demonstrated that mitochondrial dysfunction greatly amplified the damage caused by reactive oxygen species (ROS) to tumor, which strongly confirms the synergistic effect between calcium overload and reactive oxygen therapy. Conclusion Collectively, the development of CTCH presents a novel therapeutic strategy for tumor treatment by effectively responding to the acidic TME, thus holding significant clinical implications.

show abstract

Mitochondria, pattern recognition receptors and autophagy under physiological and pathological conditions, including viral infections

Cited by 2 publications

References 61 publications

A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness

A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness

Layer-by-Layer Nanoparticles for Calcium Overload in situ Enhanced Reactive Oxygen Oncotherapy

Contact Info

Product

Resources

About