High glucose inhibits proliferation and differentiation of osteoblast in alveolar bone by inducing pyroptosis

Yang, Lina; Liu, Jing; Shan, Qiusheng; Geng, Guannan; Shao, Ping

doi:10.1016/j.bbrc.2019.11.080

Cited by 47 publications

(36 citation statements)

References 28 publications

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“…Resveratrol, a TXNIP inhibitor, decreases the expression of NLRP3 and caspase1 to contribute to therapy of early onset preeclampsia pathology [18]. Clinically, high glucose activates pyroptosis through the caspase1/GSDMD/IL-1β pathway to release proinflammatory cytokines, repressing the proliferation and differentiation of osteoblast in alveolar bone, and Ac-YVAD-CMK, a caspase1 inhibitor, can reverse expression of these proteins and attenuate the formation of periodontal diseases [62]. The expression of caspase1, GSDMD, IL-18 and IL-1β increase significantly in the endothelial cells of subablated hepatic hemangioma in thirty-two patients after radiofrequency ablation, and the caspase-1-associated endothelial pyroptosis is induced by subablative hyperthermia and Ac-YVAD-CMK attenuates pyroptosis in vitro experiments [70].…”

Section: Compounds Inhibiting Pyroptosis To Treat Inflammatory Diseasesmentioning

confidence: 99%

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Zheng

2020

IJMS

139

111

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Programmed Cell Death (PCD) is considered to be a pathological form of cell death when mediated by an intracellular program and it balances cell death with survival of normal cells. Pyroptosis, a type of PCD, is induced by the inflammatory caspase cleavage of gasdermin D (GSDMD) and apoptotic caspase cleavage of gasdermin E (GSDME). This review aims to summarize the latest molecular mechanisms about pyroptosis mediated by pore-forming GSDMD and GSDME proteins that permeabilize plasma and mitochondrial membrane activating pyroptosis and apoptosis. We also discuss the potentiality of pyroptosis as a therapeutic target in human diseases. Blockade of pyroptosis by compounds can treat inflammatory disease and pyroptosis activation contributes to cancer therapy.

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Section: Compounds Inhibiting Pyroptosis To Treat Inflammatory Diseasesmentioning

confidence: 99%

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Zheng

2020

IJMS

139

111

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“…Indeed, it was suggested that the injury in bone marrow stromal cells resulted from chemotherapy could be regulated by ferroptosis, which offers an amenable target to decrease the side effects of ferroptosis initiaters 168 . In addition, it has also been demonstrated both in human and murine model that pyroptosis, a novel programmed cell death, has a pivotal role in inflammatory-related bone diseases with bone loss, such as osteomyelitis 169 and diabetes mellitus-associated periodontitis 170 , which may be due to inhibition of proliferation and differentiation of osteoblasts. Nevertheless, whether the mechanism of ferroptosis or pyroptosis could occur in osteocytes remains ill-defined.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Osteocyte apoptosis: the roles and key molecular mechanisms in resorption-related bone diseases

Wang

2020

Cell Death Dis

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Vital osteocytes have been well known to function as an important orchestrator in the preservation of robustness and fidelity of the bone remodeling process. Nevertheless, some key pathological factors, such as sex steroid deficiency and excess glucocorticoids, and so on, are implicated in inducing a bulk of apoptotic osteocytes, subsequently resulting in resorption-related bone loss. As much, osteocyte apoptosis, under homeostatic conditions, is in an optimal state of balance tightly controlled by pro- and anti-apoptotic mechanism pathways. Importantly, there exist many essential signaling proteins in the process of osteocyte apoptosis, which has a crucial role in maintaining a homeostatic environment. While increasing in vitro and in vivo studies have established, in part, key signaling pathways and cross-talk mechanism on osteocyte apoptosis, intrinsic and complex mechanism underlying osteocyte apoptosis occurs in various states of pathologies remains ill-defined. In this review, we discuss not only essential pro- and anti-apoptotic signaling pathways and key biomarkers involved in these key mechanisms under different pathological agents, but also the pivotal role of apoptotic osteocytes in osteoclastogenesis-triggered bone loss, hopefully shedding new light on the attractive and proper actions of pharmacotherapeutics of targeting apoptosis and ensuing resorption-related bone diseases such as osteoporosis and fragility fractures.

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“…The hyperglycemia environment significantly affects bone‐related cells in multiple ways. It is reported that high glucose concentration inhibits proliferation and differentiation of osteoblast, [ 26 ] reduces the osteogenic potential of bone marrow MSCs, [ 27 ] and adipose‐tissue‐derived MSCs. [ 28 ] Therefore, the reduction of glucose concentration in diabetic bone defects would be highly beneficial for bone regeneration.…”

Section: Discussionmentioning

confidence: 99%

3D Printed Enzyme‐Functionalized Scaffold Facilitates Diabetic Bone Regeneration

Yang

Zheng

Younis

et al. 2021

Adv Funct Materials

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Patients with diabetes mellitus (DM) suffer from a high risk of fractures and poor bone healing ability. Surprisingly, no effective therapy is available to treat diabetic bone defect in clinic. Here, a 3D printed enzyme‐functionalized scaffold with multiple bioactivities including osteogenesis, angiogenesis, and anti‐inflammation in diabetic conditions is proposed. The as‐prepared multifunctional scaffold is constituted with alginate, glucose oxidase (GOx), and catalase‐assisted biomineralized calcium phosphate nanosheets (CaP@CAT NSs). The GOx inside scaffolds can alleviate the hyperglycemia environment by catalyzing glucose and oxygen into gluconic acid and hydrogen peroxide (H2O2). Both the generated H2O2 as well as the overproduced H2O2 in DM can be scavenged by CaP@CAT NSs, while the initiated hypoxic microenvironment stimulates neovascularization. Moreover, the incorporation of CaP@CAT NSs not only enhance the mechanical property of the scaffolds, but also facilitate bone regeneration by the degraded Ca2+ and PO43− ions. The remarkable in vitro and in vivo outcomes demonstrate that enzymes functionalized scaffolds can be an effective strategy for enhancing bone tissue regeneration in diabetic conditions, underpinning the potential of multifunctional scaffolds for diabetic bone regeneration.

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High glucose inhibits proliferation and differentiation of osteoblast in alveolar bone by inducing pyroptosis

Cited by 47 publications

References 28 publications

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Mechanisms and Therapeutic Regulation of Pyroptosis in Inflammatory Diseases and Cancer

Osteocyte apoptosis: the roles and key molecular mechanisms in resorption-related bone diseases

3D Printed Enzyme‐Functionalized Scaffold Facilitates Diabetic Bone Regeneration

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