HMGB1-mediated apoptosis and autophagy in ischemic heart diseases

Foglio, Eleonora; Pellegrini, Laura; Germani, Antonia; Russo, Matteo Antonio

doi:10.1530/vb-19-0013

Cited by 26 publications

(19 citation statements)

References 42 publications

(57 reference statements)

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“…As mentioned above, HMGB1 acts as a damage-associated molecular pattern which is released either from necrotic cells or by secretion from activated immune cells, hepatocytes, enterocytes, and possibly several other types of cells under distress[ 107 ]. Stress conditions that promote HMGB1 secretion include hypoxia[ 108 ], lethal irradiation[ 109 ], treatment with specific antitumor drugs[ 110 ] or through regulation of autophagy[ 111 ]. HMGB1-induced cell migration requires both IκB kinase (IKK)-β and IKKα-dependent nuclear factor-κB (NF-κB) activation.…”

Section: Hmgb1-sdf1-cxcr4 Axis In Facilitating Tissue-specific Migratmentioning

confidence: 99%

Role of the CXCR4-SDF1-HMGB1 pathway in the directional migration of cells and regeneration of affected organs

Haque

Fareez

Fong

et al. 2020

WJSC

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In recent years, several studies have reported positive outcomes of cell-based therapies despite insufficient engraftment of transplanted cells. These findings have created a huge interest in the regenerative potential of paracrine factors released from transplanted stem or progenitor cells. Interestingly, this notion has also led scientists to question the role of proteins in the secretome produced by cells, tissues or organisms under certain conditions or at a particular time of regenerative therapy. Further studies have revealed that the secretomes derived from different cell types contain paracrine factors that could help to prevent apoptosis and induce proliferation of cells residing within the tissues of affected organs. This could also facilitate the migration of immune, progenitor and stem cells within the body to the site of inflammation. Of these different paracrine factors present within the secretome, researchers have given proper consideration to stromal cell-derived factor-1 (SDF1) that plays a vital role in tissue-specific migration of the cells needed for regeneration. Recently researchers recognized that SDF1 could facilitate site-specific migration of cells by regulating SDF1-CXCR4 and/or HMGB1-SDF1-CXCR4 pathways which is vital for tissue regeneration. Hence in this study, we have attempted to describe the role of different types of cells within the body in facilitating regeneration while emphasizing the HMGB1-SDF1-CXCR4 pathway that orchestrates the migration of cells to the site where regeneration is needed.

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Section: Hmgb1-sdf1-cxcr4 Axis In Facilitating Tissue-specific Migratmentioning

confidence: 99%

Role of the CXCR4-SDF1-HMGB1 pathway in the directional migration of cells and regeneration of affected organs

Haque

Fareez

Fong

et al. 2020

WJSC

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“…It seems that autophagy is a cytoprotective mechanism against cell death. Nevertheless, autophagy might also become harmful and promote cell death under specific conditions [ 27 ]. The role of autophagy in DOX-induced myocardial injury has been widely debated.…”

Section: Discussionmentioning

confidence: 99%

“…Yao et al found that HMGB1 was involved in DOX-induced cardiomyocyte apoptosis and cardiac insufficiency, and inhibiting HMGB1 could alleviate DOX-induced cardiomyopathy [ 20 ]. In addition, HMGB1 could directly interact with Beclin1 and ATG5 and block their calpain-mediated cleavage during inflammation, thereby maintaining proautophagic functions [ 27 ]. In this study, we demonstrated that the expression of HMGB1 was increased after DOX treatment, while the level of HMGB1 was reduced with miR-204 supplementation in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1

Liu

Zhao

et al. 2020

Oxidative Medicine and Cellular Longevity

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The toxicity of doxorubicin (DOX) limits its clinical application. Nevertheless, at present, there is no effective drug to prevent DOX-induced cardiac injury. miR-204 is a newly discovered miRNA with many protective effects on cardiovascular diseases. However, little research has been done on the effects of miR-204 on DOX-induced cardiac injury. Our study is aimed at investigating the effect of miR-204 on DOX-induced myocardial injury. An adenoassociated virus system was used to achieve cardiac-specific overexpression of miR-204. Two weeks later, the mice were intraperitoneally injected with DOX (15 mg/kg) to induce cardiac injury. H9c2 myocardial cells were used to validate the role of miR-204 in vitro. Our study showed that miR-204 expression was decreased in DOX-treated hearts. miR-204 overexpression improved cardiac function and alleviated cardiac inflammation, apoptosis, and autophagy induced by DOX. In addition, our results showed that miR-204 prevented DOX-induced injury in cardiomyocytes by directly decreasing HMGB1 expression. Moreover, the overexpression of HMGB1 could offset the protective effects of miR-204 against DOX-induced cardiac injury. In summary, our study showed that miR-204 protected against DOX-induced cardiac injury via the inhibition of HMGB1, and increasing miR-204 expression may be a new treatment option for patients with DOX-induced cardiac injury.

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“…There is a mutual regulation where one's inhibition affects the release of the other (Zhang et al, 2017), while uncontrolled autophagy increases the HMGB1 release (Tang et al, 2010b;Kim et al, 2020). HMGB1 is crucial for normal autophagy functioning (Tang et al, 2010a;Foglio et al, 2019). As a transcriptional co-factor, HMGB1 regulates the expression of heat shock protein β-1 (Tang et al, 2011;Foglio et al, 2019), which sustains dynamic intracellular trafficking during autophagy.…”

Section: Hmgb1 Autophagy and Mets: A Suggestive Triangulationmentioning

confidence: 99%

Metabolic Syndrome and Autophagy: Focus on HMGB1 Protein

Frisardi

Matrone

Street³

2021

Front. Cell Dev. Biol.

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Metabolic syndrome (MetS) affects the population worldwide and results from several factors such as genetic background, environment and lifestyle. In recent years, an interplay among autophagy, metabolism, and metabolic disorders has become apparent. Defects in the autophagy machinery are associated with the dysfunction of many tissues/organs regulating metabolism. Metabolic hormones and nutrients regulate, in turn, the autophagy mechanism. Autophagy is a housekeeping stress-induced degradation process that ensures cellular homeostasis. High mobility group box 1 (HMGB1) is a highly conserved nuclear protein with a nuclear and extracellular role that functions as an extracellular signaling molecule under specific conditions. Several studies have shown that HMGB1 is a critical regulator of autophagy. This mini-review focuses on the involvement of HMGB1 protein in the interplay between autophagy and MetS, emphasizing its potential role as a promising biomarker candidate for the early stage of MetS or disease’s therapeutic target.

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HMGB1-mediated apoptosis and autophagy in ischemic heart diseases

Cited by 26 publications

References 42 publications

Role of the CXCR4-SDF1-HMGB1 pathway in the directional migration of cells and regeneration of affected organs

Role of the CXCR4-SDF1-HMGB1 pathway in the directional migration of cells and regeneration of affected organs

Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1

Metabolic Syndrome and Autophagy: Focus on HMGB1 Protein

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