Focal Adhesion Kinase Activity and Localization is Critical for TNF-α-Induced Nuclear Factor-κB Activation

Murphy, James M.; Jeong, Kyuho; Cioffi, Donna L.; Campbell, Pamela Moore; Jo, Hanjoong; Ahn, Eun-Young; Lim, Ssang‐Taek

doi:10.1007/s10753-020-01408-5

Cited by 7 publications

(6 citation statements)

References 40 publications

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“…Interestingly, we found that the proteins that were specifically upregulated in the atria of HF samples were mainly enriched in the complement and coagulation cascades, which cause overt inflammation, thrombotic microangiopathy and end-organ damage [ 32 – 34 ]; however, the proteins that were specifically upregulated in the ventricles of HF samples were mainly enriched in the FoxO signaling pathway, which is involved in maintaining cardiomyocytes in the homeostatic state and inducing their adaptation to metabolism [ 35 , 36 ], and the apelin signaling pathway, which plays a critical role in the positive inotropic effect and maintains cardiac contractility [ 37 , 38 ]. The proteins that were specifically downregulated in the atria of HF samples were mainly enriched in the tight junction and focal adhesion signaling pathways, indicating endothelial dysfunction and cardiac inflammation [ 39 , 40 ]. These findings suggest that inflammation may occur in the atria in the early stage of HF and that activation of FoxO and apelin signaling pathways in the ventricles represents an attempt to maintain cardiac contractility.…”

Section: Discussionmentioning

confidence: 99%

GSTM2 alleviates heart failure by inhibiting DNA damage in cardiomyocytes

Xu,

Wang,

Wang

et al. 2023

Cell Biosci

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Background Heart failure (HF) seriously threatens human health worldwide. However, the pathological mechanisms underlying HF are still not fully clear. Results In this study, we performed proteomics and transcriptomics analyses on samples from human HF patients and healthy donors to obtain an overview of the detailed changes in protein and mRNA expression that occur during HF. We found substantial differences in protein expression changes between the atria and ventricles of myocardial tissues from patients with HF. Interestingly, the metabolic state of ventricular tissues was altered in HF samples, and inflammatory pathways were activated in atrial tissues. Through analysis of differentially expressed genes in HF samples, we found that several glutathione S-transferase (GST) family members, especially glutathione S-transferase M2-2 (GSTM2), were decreased in all the ventricular samples. Furthermore, GSTM2 overexpression effectively relieved the progression of cardiac hypertrophy in a transverse aortic constriction (TAC) surgery-induced HF mouse model. Moreover, we found that GSTM2 attenuated DNA damage and extrachromosomal circular DNA (eccDNA) production in cardiomyocytes, thereby ameliorating interferon-I-stimulated macrophage inflammation in heart tissues. Conclusions Our study establishes a proteomic and transcriptomic map of human HF tissues, highlights the functional importance of GSTM2 in HF progression, and provides a novel therapeutic target for HF.

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Section: Discussionmentioning

confidence: 99%

GSTM2 alleviates heart failure by inhibiting DNA damage in cardiomyocytes

Xu,

Wang,

Wang

et al. 2023

Cell Biosci

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“…FAK can translocate to the nucleus and modulate the expression of genes related to inflammation such as chemokines and cytokines and the secretion of ECM molecules like collagens thereby impacting the composition of the ECM [ 271 ]. Consequently, FAK can serve as a mediator for both inflammatory and physical signals in AD [ 273 ].…”

Section: Consideration Of Nz@hydrogels With Mechanobiological Functionsmentioning

confidence: 99%

Nanozyme-Engineered Hydrogels for Anti-Inflammation and Skin Regeneration

Kurian,

Singh,

Sagar

et al. 2024

Nano-Micro Lett.

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Inflammatory skin disorders can cause chronic scarring and functional impairments, posing a significant burden on patients and the healthcare system. Conventional therapies, such as corticosteroids and nonsteroidal anti-inflammatory drugs, are limited in efficacy and associated with adverse effects. Recently, nanozyme (NZ)-based hydrogels have shown great promise in addressing these challenges. NZ-based hydrogels possess unique therapeutic abilities by combining the therapeutic benefits of redox nanomaterials with enzymatic activity and the water-retaining capacity of hydrogels. The multifaceted therapeutic effects of these hydrogels include scavenging reactive oxygen species and other inflammatory mediators modulating immune responses toward a pro-regenerative environment and enhancing regenerative potential by triggering cell migration and differentiation. This review highlights the current state of the art in NZ-engineered hydrogels (NZ@hydrogels) for anti-inflammatory and skin regeneration applications. It also discusses the underlying chemo-mechano-biological mechanisms behind their effectiveness. Additionally, the challenges and future directions in this ground, particularly their clinical translation, are addressed. The insights provided in this review can aid in the design and engineering of novel NZ-based hydrogels, offering new possibilities for targeted and personalized skin-care therapies.

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“… 22 Furthermore, recent studies demonstrated FAK to be a versatile scaffold that can localize in the nucleus and control gene transcription and cellular functions in a kinase-independent manner. 23 , 24 Thus, precisely how FAK functions to govern EC-restrictive fate remains to be seen.…”

Section: Introductionmentioning

confidence: 99%

FAK regulates tension transmission to the nucleus and endothelial transcriptome independent of kinase activity

Akhter,

Yazbeck,

Tauseef

et al. 2024

Cell Reports

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Focal Adhesion Kinase Activity and Localization is Critical for TNF-α-Induced Nuclear Factor-κB Activation

Cited by 7 publications

References 40 publications

GSTM2 alleviates heart failure by inhibiting DNA damage in cardiomyocytes

GSTM2 alleviates heart failure by inhibiting DNA damage in cardiomyocytes

Nanozyme-Engineered Hydrogels for Anti-Inflammation and Skin Regeneration

FAK regulates tension transmission to the nucleus and endothelial transcriptome independent of kinase activity

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