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The Editor of Molecular Medicine Reports has agreed that the paper should be retracted; moreover, the authors apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 22 4351-4359, 2020; DOI 10.3892/mmr.2020.11501].Induction of cardiomyocyte (CM) proliferation is a promising approach for cardiac regeneration following myocardial injury. MicroRNAs (miRs) have been reported to regulate CM proliferation. In particular, miR‑449a‑5p has been identified to be associated with CM proliferation in previous high throughput functional screening data. However, whether miR‑449a‑5p regulates CM proliferation has not been thoroughly investigated. This study aimed to explore whether miR‑449a‑5p modulates CM proliferation and to identify the molecular mechanism via which miR‑449a‑5p regulates CM proliferation. The current study demonstrated that miR‑449a‑5p expression levels were significantly increased during heart development. Furthermore, the results suggested that miR‑449a‑5p mimic inhibited CM proliferation as determined via immunofluorescence for ki67 and histone H3 phosphorylated at serine 10 (pH3), as well as the numbers of CMs. However, miR‑449a‑5p knockdown promoted CM proliferation. CDK6 was identified as a direct target gene of miR‑449a‑5p, and CDK6 mRNA and protein expression was suppressed by miR‑449a‑5p. Moreover, CDK6 gain‑of‑function increased CM proliferation. Overexpression of CDK6 also blocked the inhibitory effect of miR‑449a‑5p on CM proliferation, indicating that CDK6 was a functional target of miR‑449a‑5p in CM proliferation. In conclusion, miR‑449a‑5p inhibited CM proliferation by targeting CDK6, which provides a potential molecular target for preventing myocardial injury.Huangqi, the dried root of Radix Astragali, is an essential herb in Traditional Chinese Medicine and has been used to promote hematopoiesis for centuries. Astragalus polysaccharide (ASPS), the bioactive compound of Huangqi, serves a crucial role in hematopoiesis. The aim of the present study was to investigate the hematopoietic effects, in particular the thrombopoietic effects, and the molecular mechanisms of ASPS using an irradiation‑induced myelosuppressive mouse model. Colony‑forming unit assays, flow cytometric analysis of apoptosis, ELISAs, Giemsa staining and western blotting were performed to determine the hematopoietic and anti‑apoptotic effects of ASPS. The results demonstrated that ASPS enhanced the recovery of red blood cells at day 21 following treatment, as well as platelets and white blood cells at day 14. In addition, ASPS promoted colony formation in all lineages (megakaryocytes, granulocyte monocytes, erythroid cells and fibroblasts). The morphological study of the bone marrow demonstrated that tri‑lineage hematopoiesis was preserved in the ASPS‑ and thrombopoietin (TPO)‑treated groups compared with the control group. The overall cellularity (mean total cell count/area) of the ASPS‑treated group was similar to that of the TPO‑treated group. Additionally, g/ml ASPS exhibited the maximum effect on colony formation. ASPS attenuated cell apoptosis in megakaryocytic cells via inhibiting the mitochondrial caspase‑3 signaling pathway. In conclusion, ASPS promoted hematopoiesis in irradiated myelosuppressive mice possibly via enhancing hematopoietic stem/progenitor cell proliferation and inhibiting megakaryocytes apoptosis.It has been reported that sevoflurane induces neurotoxicity in the developing brain. Dexmedetomidine is an α2 adrenoceptor agonist used for the prevention of sevoflurane‑induced agitation in children in clinical practice. The aim of the present study was to determine whether dexmedetomidine could prevent sevoflurane‑induced neuroapoptosis, neuroinflammation, oxidative stress and neurocognitive impairment. Additionally, the involvement of α2 adrenoceptors in the neuroprotective effect of dexmedetomidine was assessed. Postnatal day (P)6 C57BL/6 male mice were randomly divided into four groups (n=6 in each group). Mice were pretreated with dexmedetomidine, either alone or together with yohimbine, an α2 adrenoceptor inhibitor, then exposed to 3% sevoflurane in 25% oxygen. Control mice either received normal saline alone or with sevoflurane exposure. Following sevoflurane exposure, the expression of cleaved caspase‑3 was detected by immunohistochemistry in hippocampal tissue sections. In addition, the levels of tue impairment, which was mediated, at least in part, by α2 adrenoceptors.Acute myocardial infarction (AMI) is a common cardiac disease. Long non‑coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia‑inducible factor 1α (HIF1α), MEG3, microRNA (miR)‑325‑3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia‑treated H9c2 cells were detected via reverse transcription‑quantitative PCR. The protein expression levels of HIF1α, Bcl‑2, Bax, cleaved caspase‑3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual‑luciferase reporter assay was performed to verify the targeted relationship between miR‑325‑3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR‑325‑3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR‑325‑3p was downregulated by MEG3 compared with the vector group, and miR‑325‑3p targeted TRPV4 in hypoxia‑treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia‑stimulated injury in H9c2 cells by regulating miR‑325‑3p. TRPV4 knockdown also mitigated hypoxia‑induced injury in H9c2 cells via miR‑325‑3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia‑treated H9c2 cells by sponging miR‑325‑3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia‑induced injury in rat cardiomyocytes by sponging miR‑325‑3p.Lipid accumulation in podocytes can lead to the destruction of cellular morphology, in addition to cell dysfunction and apoptosis, which is a key factor in the progression of chronic kidney disease (CKD). Berberine (BBR) is an isoquinoline alkaloid extracted from medicinal plants such as model. Cell death was measured using the Cell Counting Kit‑8 colorimetric assay. Cell apoptotic rate was assessed by flow cytometry. The expression of endoplasmic reticulum (ER) stress‑ and apoptosis‑related proteins was detected by western blotting or immunofluorescence. Reactive oxygen species (ROS) were evaluated by 2',7'‑dichlorofluorescein diacetate fluorescence staining. The results of the present study revealed that BBR treatment decreased PA‑induced podocyte apoptosis. In addition, 4‑phenylbutyric acid significantly reduced PA‑induced cell apoptosis and the expression of ER stress‑related proteins, which indicated that ER stress was involved in PA‑induced podocyte apoptosis. In addition, N‑acetylcysteine inhibited PA‑induced excessive ROS production, ER stress and cell apoptosis of podocytes. BBR also significantly reduced PA‑induced ROS production and ER stress in podocytes. These results suggested that PA mediated podocyte apoptosis through enhancing ER stress and the production of ROS. In conclusion, BBR may protect against PA‑induced podocyte apoptosis, and suppression of ROS‑dependent ER stress may be the key mechanism underlying the protective effects of BBR.While there are numerous small molecule inhibitory drugs available for a wide range of signalling pathways, at present, they are generally not used in combination in clinical settings. Previous reports have reported that the effects of glycogen synthase kinase (GSK)3β, p38MAPK, mTOR and histone deacetylase signaling combined together to suppress the stem‑like nature of hematopoietic stem cells (HSCs), driving these cells to differentiate, cease proliferating and thereby impairing normal hematopoietic functionality. The present study aimed to determine the effect of HDACs, mTOR, GSK‑3β and p38MAPK inhibitor combinations on the efficient expansion of HSCs using flow cytometry. Moreover, it specifically aimed to determine how inhibitors of the GSK3β signaling pathway, in combination with inhibitors of P38MAPK and mTOR signaling or histone deacetylase (HDAC) inhibitors, could affect HSC expansion, with the goal of identifying novel combination strategies useful for the expansion of HSCs. The results indicated that p38MAPK and/or GSK3β inhibitors increased Lin‑ cell and Lin‑Sca‑1+c‑kit+ (LSK) cell numbers . These findings further indicated that the suppression of p38MAPK and/or GSK3β signalling may modulate HSC differentiation and self‑renewal to enhance HSC expansion.Increasing evidence has demonstrated that long non‑coding RNAs (lncRNAs) serve important roles in numerous malignancies, including triple‑negative breast cancer (TNBC). The lncRNA titin‑antisense RNA1 (TTN‑AS1) has previously been reported to promote tumorigenesis in various types of cancer. The present study aimed to investigate the potential role of TTN‑AS1 in breast cancer and the associated underlying mechanisms. Following prediction by Starbase and confirmation by dual‑luciferase reporter assay, TINCR was demonstrated to be a target gene for microRNA (miR)‑211‑5p. The expression levels of TTN‑AS1 and miR‑211‑5p, which was predicted to be targeted by TTN‑AS1, in TNBC tissues and in the breast cancer cell lines MDA‑MB‑453 and MDA‑MB‑231 were measured using reverse transcription‑quantitative PCR. Following TTN‑AS1‑knockdown, cell proliferation was measured using a Cell Counting Kit‑8 assay and colony formation assay, whereas cell invasion and migration were measured using Transwell and wound healing assays,ion and invasive and migratory abilities of TNBC by targeting miR‑211‑5p. This study may provide some insights into the regulatory mechanism of TNBC and help the development of novel therapeutic interventions for TNBC.Platelets are small pieces of cytoplasm that have become detached from the cytoplasm of mature megakaryocytes (MKs) in the bone marrow. Platelets modulate vascular system integrity and serve important role, particularly in hemostasis. With the rapid development of clinical medicine, the demand for platelet transfusion as a life‑saving intervention increases continuously. Stem cell technology appears to be highly promising for transfusion medicine, and the generation of platelets from stem cells would be of great value in the clinical setting. Furthermore, several studies have been undertaken to investigate the potential of producing platelets from stem cells. Initial success has been achieved in terms of the yields and function of platelets generated from stem cells. However, the requirements of clinical practice remain unmet. The aim of the present review was to focus on several sources of stem cells and factors that induce MK differentiation. Updated information on current research into the genetic regulation of megakaryocytopoiesis and platelet generation was summarized.