An update of current therapeutic approach for Intervertebral Disc Degeneration: A review article

Romaniyanto,; Mahyudin, Ferdiansyah; Prakoeswa, Cita Rosita Sigit; Notobroto, Hari Basuki; Tinduh, Damayanti; Ausrin, Ryan; Rantam, Fedik Abdul; Suroto, Heri; Utomo, Dwikora Novembri; Рhatomy, Сholahuddin

doi:10.1016/j.amsu.2022.103619

Cited by 29 publications

(32 citation statements)

References 49 publications

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“…As primary cells residing in the nucleus pulposus (NP), NPCs are responsible for the synthesis of ECM and maintain the biological and mechanical properties of the intervertebral disc [ 70 ]. The dysfunction of NP tissue plays a crucial role in the pathological development of IVDD [ 71 ]. The intervertebral disc is the largest avascular tissue in mammals.…”

Section: Mitophagy and Intervertebral Disc Degenerationmentioning

confidence: 99%

Mitophagy—A New Target of Bone Disease

et al. 2022

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Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.

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Section: Mitophagy and Intervertebral Disc Degenerationmentioning

confidence: 99%

Mitophagy—A New Target of Bone Disease

et al. 2022

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“…Anatomically, the IVD is a large and avascular fibrocartilaginous tissue located between every two neighboring vertebrae. It consists of three main parts: the central nucleus pulpous (NP), surrounding collagenous annulus fibrous (AF), and the two cartilaginous endplates (CEP) that separate AF and NP from the vertebral bodies [ 16 , 17 , 18 , 19 , 20 ]. NP is the hydrophilic core of IVD, composed of collagen II and elastin fibers embedded in an aggrecan-containing gel.…”

Section: Pathogenesis and Etiology Of Intervertebral Disc Degenerationmentioning

confidence: 99%

“…Intervertebral disc degeneration (IDD) is a multifactorial process that can result from various causes, counting aging, injury, wrong posture, abnormal loading, and environmental and genetic factors [ 20 , 21 ]. The disappearance of large vacuolated notochordal cells in NP around the age of 10 and the calcification of the CEPs are two processes that initiate and exacerbate IDD [ 17 ]. The degenerative cascade is frequently triggered by an imbalance between catabolic and anabolic processes in the IVDs [ 22 ].…”

Section: Pathogenesis and Etiology Of Intervertebral Disc Degenerationmentioning

confidence: 99%

“…Pain reliever medication is given to patients with symptomatic degenerative disc disease, but it only works in the short term, decreasing inflammation and providing temporary anesthesia in the area where the irritated nerve is involved [ 17 ]. To achieve longer-term results and better outcomes, the focus must be directed to the factors driving the pathological alterations.…”

Section: Strategies For Managing Intervertebral Disc Degenerationmentioning

confidence: 99%

“…As it has been observed that reduced growth factor supply at the level of IVD increases the rate of disc cell senescence, the administration of growth factors began to be considered a potential therapeutic strategy. Injecting various growth factors (e.g., members of the transforming growth factor-β (TGF-β) superfamily, IGF-1, growth differentiation factor 5 (GDF-5), BMP-2, BMP-7, and platelet-derived growth factor (PDGF)) into the IVD can stimulate ECM synthesis, prevent cell senescence induced by oxidative stress, relieve inflammation, restore the balance of anabolic and catabolic activities, and delay the degeneration process [ 13 , 17 , 18 , 89 ]. In more detail, TGF-β1 and TGF-β3 can induce discogenic differentiation, direct cells towards a fibrocartilaginous phenotype, and reduce the damage caused by degeneration.…”

Section: Strategies For Managing Intervertebral Disc Degenerationmentioning

confidence: 99%

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Recent Advances in Managing Spinal Intervertebral Discs Degeneration

Costăchescu

Niculescu

Teleanu

et al. 2022

IJMS

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Low back pain (LBP) represents a frequent and debilitating condition affecting a large part of the global population and posing a worldwide health and economic burden. The major cause of LBP is intervertebral disc degeneration (IDD), a complex disease that can further aggravate and give rise to severe spine problems. As most of the current treatments for IDD either only alleviate the associated symptoms or expose patients to the risk of intraoperative and postoperative complications, there is a pressing need to develop better therapeutic strategies. In this respect, the present paper first describes the pathogenesis and etiology of IDD to set the framework for what has to be combated to restore the normal state of intervertebral discs (IVDs), then further elaborates on the recent advances in managing IDD. Specifically, there are reviewed bioactive compounds and growth factors that have shown promising potential against underlying factors of IDD, cell-based therapies for IVD regeneration, biomimetic artificial IVDs, and several other emerging IDD therapeutic options (e.g., exosomes, RNA approaches, and artificial intelligence).

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Hypoxia‐Preconditioned BMSC‐Derived Exosomes Induce Mitophagy via the BNIP3–ANAX2 Axis to Alleviate Intervertebral Disc Degeneration

Jin,

Wu,

Chen

et al. 2024

Advanced Science

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Intervertebral disc degeneration (IVDD) is a chronic degenerative disease involving the aging and loss of proliferative capacity of nucleus pulposus cells (NPCs), processes heavily dependent on mitochondrial dynamics and autophagic flux. This study finds that the absence of BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) is associated with senescence‐related NPC degeneration, disrupting mitochondrial quality control. Bone marrow mesenchymal stem cells (BMSCs) have multidirectional differentiation potential and produce extracellular vesicles containing cellular activators. Therefore, in this study, BMSCs are induced under hypoxic stimulation to deliver BNIP3‐rich extracellular vesicles to NPCs, thereby alleviating aging‐associated mitochondrial autophagic flux, promoting damaged mitochondrial clearance, and restoring mitochondrial quality control. Mechanistically, BNIP3 is shown to interact with the membrane‐bound protein annexin A2 (ANXA2), enabling the liberation of the transcription factor EB (TFEB) from the ANXA2‐TFEB complex, promoting TFEB nuclear translocation, and regulating autophagy and lysosomal gene activation. Furthermore, a rat model of IVDD is established and verified the in vivo efficacy of the exosomes in repairing disc injuries, delaying NPC aging, and promoting extracellular matrix (ECM) synthesis. In summary, hypoxia‐induced BMSC exosomes deliver BNIP3‐rich vesicles to alleviate disc degeneration by activating the mitochondrial BNIP3/ANXA2/TFEB axis, providing a new target for IVDD treatment.

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An update of current therapeutic approach for Intervertebral Disc Degeneration: A review article

Cited by 29 publications

References 49 publications

Mitophagy—A New Target of Bone Disease

Mitophagy—A New Target of Bone Disease

Recent Advances in Managing Spinal Intervertebral Discs Degeneration

Hypoxia‐Preconditioned BMSC‐Derived Exosomes Induce Mitophagy via the BNIP3–ANAX2 Axis to Alleviate Intervertebral Disc Degeneration

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