| HDAC4 represses ER stress induced chondrocyte apoptosis by inhibiting ATF4 and attenuates cartilage degeneration in an osteoarthritis rat model. | HDAC4 represses ER stress induced chondrocyte apoptosis by inhibiting ATF4 and attenuates cartilage degeneration in an osteoarthritis rat model.
Gu X, Li F, Che X, Wei X, Li P., Free PMC Article | 07/1/2024 |
| Urine-derived stem cells-extracellular vesicles ameliorate diabetic osteoporosis through HDAC4/HIF-1alpha/VEGFA axis by delivering microRNA-26a-5p. | Urine-derived stem cells-extracellular vesicles ameliorate diabetic osteoporosis through HDAC4/HIF-1α/VEGFA axis by delivering microRNA-26a-5p.
Zhang D, Du J, Yu M, Suo L. | 10/30/2023 |
| Role of Glucocorticoid Signaling and HDAC4 Activation in Diaphragm and Gastrocnemius Proteolytic Activity in Septic Rats. | Role of Glucocorticoid Signaling and HDAC4 Activation in Diaphragm and Gastrocnemius Proteolytic Activity in Septic Rats.
Moreno-Rupérez Á, Priego T, González-Nicolás MÁ, López-Calderón A, Lázaro A, Martín AI., Free PMC Article | 04/30/2022 |
| Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis. | Butyrate-containing structured lipids act on HDAC4, HDAC6, DNA damage and telomerase activity during promotion of experimental hepatocarcinogenesis.
Festa Ortega JF, Heidor R, Auriemo AP, Marques Affonso J, Pereira D' Amico T, Herz C, de Conti A, Ract J, Gioieli LA, Purgatto E, Lamy E, P Pogribny I, Salvador Moreno F. | 12/25/2021 |
| HDAC4 induces the development of asthma by increasing Slug-upregulated CXCL12 expression through KLF5 deacetylation. | HDAC4 induces the development of asthma by increasing Slug-upregulated CXCL12 expression through KLF5 deacetylation.
Wei W, Chen W, He N., Free PMC Article | 09/11/2021 |
| Beneficial Effects of a Mixture of Algae and Extra Virgin Olive Oils on the Age-Induced Alterations of Rodent Skeletal Muscle: Role of HDAC-4. | Beneficial Effects of a Mixture of Algae and Extra Virgin Olive Oils on the Age-Induced Alterations of Rodent Skeletal Muscle: Role of HDAC-4.
González-Hedström D, Priego T, López-Calderón A, Amor S, de la Fuente-Fernández M, Inarejos-García AM, García-Villalón ÁL, Martín AI, Granado M., Free PMC Article | 09/4/2021 |
| Leucine Supplementation Decreases HDAC4 Expression and Nuclear Localization in Skeletal Muscle Fiber of Rats Submitted to Hindlimb Immobilization. | Leucine Supplementation Decreases HDAC4 Expression and Nuclear Localization in Skeletal Muscle Fiber of Rats Submitted to Hindlimb Immobilization.
Alves PKN, Cruz A, Silva WJ, Labeit S, Moriscot AS., Free PMC Article | 07/10/2021 |
| HDAC4 and HDAC5 form a complex with DREAM that epigenetically down-regulates NCX3 gene and its pharmacological inhibition reduces neuronal stroke damage. | HDAC4 and HDAC5 form a complex with DREAM that epigenetically down-regulates NCX3 gene and its pharmacological inhibition reduces neuronal stroke damage.
Formisano L, Laudati G, Guida N, Mascolo L, Serani A, Cuomo O, Cantile M, Boscia F, Molinaro P, Anzilotti S, Pizzorusso V, Di Renzo G, Pignataro G, Annunziato L., Free PMC Article | 03/20/2021 |
| miR-873-3p targets HDAC4 to stimulate matrix metalloproteinase-13 expression upon parathyroid hormone exposure in rat osteoblasts. | miR-873-3p targets HDAC4 to stimulate matrix metalloproteinase-13 expression upon parathyroid hormone exposure in rat osteoblasts.
Malavika D, Shreya S, Raj Priya V, Rohini M, He Z, Partridge NC, Selvamurugan N. | 03/13/2021 |
| Differences in the Role of HDACs 4 and 5 in the Modulation of Processes Regulating MAFbx and MuRF1 Expression during Muscle Unloading. | Differences in the Role of HDACs 4 and 5 in the Modulation of Processes Regulating MAFbx and MuRF1 Expression during Muscle Unloading.
Mochalova EP, Belova SP, Kostrominova TY, Shenkman BS, Nemirovskaya TL., Free PMC Article | 02/20/2021 |
| The data indicated that a single bout of preconditioning exercise prior to hindlimb unloading may exert a protective effect in disuse muscle atrophy in old rats and that these effects may be partially mediated by the HDAC4/Gadd45alpha axis. | Exercise preconditioning attenuates hind limb unloading-induced gastrocnemius muscle atrophy possibly via the HDAC4/Gadd45 axis in old rats.
Yoshihara T, Tsuzuki T, Chang SW, Kakigi R, Sugiura T, Naito H. | 07/25/2020 |
| HDAC4-mediated FoxO3a acetylation regulates Ang II-induced autophagy activation, which in turn plays an essential role in causing vascular inflammation. | HDAC4 regulates vascular inflammation via activation of autophagy.
Yang D, Xiao C, Long F, Su Z, Jia W, Qin M, Huang M, Wu W, Suguro R, Liu X, Zhu Y. | 08/17/2019 |
| Results suggest role of HDAC4-associated epigenetics modification in the spinal plasticity underlying pain hypersensitivity after inflammatory insults by altering COX2 expression in the dorsal horn. Moreover, through pGluN2B-NMDAR/pCaMKII signaling, excitation of spinal NMDARs impacts such a HDAC4-dependent COX2 expression to participate in the pathophysiology underlying development of inflammatory pain. | GluN2B/CaMKII mediates CFA-induced hyperalgesia via HDAC4-modified spinal COX2 transcription.
Lai CY, Hsieh MC, Ho YC, Chen GD, Chou D, Ruan T, Lee AS, Wang HH, Chau YP, Peng HY, Lai CH. | 02/23/2019 |
| the present study demonstrated that resveratrol attenuated AngIIinduced cell proliferation and neointimal hyperplasia by inhibiting the CaMKIIHDAC4 signaling pathway. These findings suggest that resveratrol may potentially prevent arterial restenosis. | Resveratrol inhibits angiotensin II‑induced proliferation of A7r5 cells and decreases neointimal hyperplasia by inhibiting the CaMKII‑HDAC4 signaling pathway.
Lin X, Cheng C, Zhong J, Liu B, Luo C, Ou W, Mo P, Huang Q, Liu S. | 10/20/2018 |
| These results suggest that HDAC4 and HDAC8 may serve as key upstream mediators of MAPK in regulating the IL1betainduced cartilage catabolic and degradation. | Histone deacetylase-4 and histone deacetylase-8 regulate interleukin-1β-induced cartilage catabolic degradation through MAPK/JNK and ERK pathways.
Wang P, Mao Z, Pan Q, Lu R, Huang X, Shang X, Zhang R, You H., Free PMC Article | 09/1/2018 |
| HDAC4 regulates thimerosal-induced cell death in neurons and that treatment with MC1568 prevents thimerosal-induced activation of caspase-3 in the rat prefrontal cortex. | MC1568 Inhibits Thimerosal-Induced Apoptotic Cell Death by Preventing HDAC4 Up-Regulation in Neuronal Cells and in Rat Prefrontal Cortex.
Guida N, Laudati G, Mascolo L, Cuomo O, Anzilotti S, Sirabella R, Santopaolo M, Galgani M, Montuori P, Di Renzo G, Canzoniero LM, Formisano L. | 01/20/2018 |
| the up-regulation of MMP genes is mediated through degradation of class IIa histone deacetylases (HDACs) by certain cysteine cathepsins (Cts). | Cathepsin H-Mediated Degradation of HDAC4 for Matrix Metalloproteinase Expression in Hepatic Stellate Cells: Implications of Epigenetic Suppression of Matrix Metalloproteinases in Fibrosis through Stabilization of Class IIa Histone Deacetylases.
Yang Z, Liu Y, Qin L, Wu P, Xia Z, Luo M, Zeng Y, Tsukamoto H, Ju Z, Su D, Kang H, Xiao Z, Zheng S, Duan Z, Hu R, Wang Q, Pandol SJ, Han YP., Free PMC Article | 05/27/2017 |
| Our data suggest that nuclear HDAC4 accumulation in skeletal muscle is partly related to immobilization-induced muscle atrophy. | Immobilization induces nuclear accumulation of HDAC4 in rat skeletal muscle.
Yoshihara T, Machida S, Kurosaka Y, Kakigi R, Sugiura T, Naito H., Free PMC Article | 05/6/2017 |
| Cx43 and HDAC4 mRNA expression first decreased and then increased compared to that in the control group; differences in HDAC4 mRNA expression were significant in the 1-week group. | Changes in expression of specific miRNAs and their target genes in repair of exercise-induced muscle injury in rats.
Wu W. | 02/25/2017 |
| Phosphorylation of HDAC4 was remarkably upregulated after stroke and blockade of HDAC4 phosphorylation with GO6976 repressed stroke-induced angiogenesis. Phosphorylation of HDAC4 was also increased in endothelial cells hypoxia model and suppression of HDAC4 phosphorylation inhibited the tube formation and migration of endothelial cells in vitro. | Role of Phosphorylated HDAC4 in Stroke-Induced Angiogenesis.
Liu J, Zhou X, Li Q, Zhou SM, Hu B, Hu GW, Niu X, Guo SC, Wang Y, Deng ZF., Free PMC Article | 02/18/2017 |
| Melatonin -exhibited anti-allodynia is mediated by MT2-enhanced PP2Ac expression that couples PP2Ac with HDAC4 to induce HDAC4 dephosphorylation and nuclear import, herein increases HDAC4 binding to the promoter of hmgb1 gene and upregulates HMGB1 expression in dorsal horn neurons. | Melatonin relieves neuropathic allodynia through spinal MT2-enhanced PP2Ac and downstream HDAC4 shuttling-dependent epigenetic modification of hmgb1 transcription.
Lin TB, Hsieh MC, Lai CY, Cheng JK, Wang HH, Chau YP, Chen GD, Peng HY. | 12/17/2016 |
| chromatin immunoprecipitation experiments showed that NFAT1-HDAC4 or NFAT3-HDAC4 complexes might be involved in regulation of PMCA2x splicing variant generation. | NFAT1 and NFAT3 cooperate with HDAC4 during regulation of alternative splicing of PMCA isoforms in PC12 cells.
Kosiorek M, Podszywalow-Bartnicka P, Zylinska L, Pikula S., Free PMC Article | 01/16/2016 |
| Neuropathic pain maintenance involves spinal HDAC4 phosphorylation and retention in dorsal horn neurons. | Modulation of Nerve Injury-induced HDAC4 Cytoplasmic Retention Contributes to Neuropathic Pain in Rats.
Lin TB, Hsieh MC, Lai CY, Cheng JK, Chau YP, Ruan T, Chen GD, Peng HY. | 11/21/2015 |
| Stroke induces nuclear shuttling of HDAC4 in neurons in the peri-infarct cortex. | Stroke Induces Nuclear Shuttling of Histone Deacetylase 4.
Kassis H, Shehadah A, Chopp M, Roberts C, Zhang ZG., Free PMC Article | 09/12/2015 |
| Thus, HDAC4 contributes to podocyte injury and is one of critical components of a signal transduction pathway that links renal injury to autophagy in diabetic nephropathy. | Histone deacetylase 4 selectively contributes to podocyte injury in diabetic nephropathy.
Wang X, Liu J, Zhen J, Zhang C, Wan Q, Liu G, Wei X, Zhang Y, Wang Z, Han H, Xu H, Bao C, Song Z, Zhang X, Li N, Yi F. | 07/4/2015 |