Abstract: Objective　To investigate the characteristics of macrophage depletion by clodronate liposomes (CL) in a carbon tetrachloride (CCl₄ )-induced liver fibrosis mouse model, and to analyze the transcriptomic features. Methods　Thirty-two C57BL/6 mice were divided randomly into plain control liposomes for clophosome (PL) and clodronate liposome (CL) groups (n=16 mice per group), and administered intraperitoneal injections of PL and CL, respectively. On day 5, each group was further divided into normal (N) and model (M) subgroups (n=8 mice per subgroup). Mice in group M received 10% CCl4 intraperitoneally to induce liver fibrosis, while mice in group N received an equal volume of olive oil. After 4 weeks, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured, and hepatic inflammation and collagen deposition were evaluated by hematoxylin/eosin and Sirius red staining, respectively. Total RNA was extracted from liver tissues for transcriptomic sequencing and subsequent differential gene expression analysis. Results　Serum ALT and AST levels were significantly elevated in the PL-M group(P<0.01), with fibrosis staging primarily at S3, compared with S1 in the CLM group. Totals of 1462 and 2119 differentially expressed genes (|log fold change|>2 and P<0.05) were identified in the PL and CL groups, respectively. Gene Ontology analysis revealed enrichment in multiple biological processes, cellular components, and molecular functions in both models, and Kyoto Encyclopedia of Genes and Genomes analysis identified 29 significantly enriched pathways (P<0.05). The upregulation of genes including Lgals7 and Timp1 and the downregulation of Mup-ps16 and Mup15 were validated by reverse transcription-quantitative polymerase chain reaction, consistent with transcriptomic trends (P<0.05). Conclusions　This study highlights the characteristics and transcriptomic features of macrophage depletion in the CCl₄-induced liver fibrosis model, providing a theoretical reference for research on the immune mechanisms of liver fibrosis.

Abstract: Objective　To investigate the efficiency and mechanism of C1q tumor necrosis factor-related protein 3 (CTRP3) on reprogramming of cardiac fibroblasts (CFs) into induced cardiomyocyte-like cells (iCMs) by Sendai virus (SeV) vector overexpressing Gata4, Mef2c and Tbx5 (SeVGMT). Methods　CFs were divided into Control, NC-Lv, CTRP3-Lv, NC-sh, and CTRP3-sh groups. NC-Lv, CTRP3-Lv, NC-sh, and CTRP3-sh were transfected into CFs using Lipofectamine 3000 reagent for 48 hours. Lipofectamine 3000 reagent was then mixed with SeVGMT and incubated at room temperature for 48 hours, the culture medium was then replaced, and cells were cultured for 21 days. Cell morphology was observed under a microscope at 0, 3, 7, 14, and 21 days. Expression levels of the myocardial-specific proteins α-myosin heavy chain (α-MHC), α-actin, cardiac troponin T (cTnT), connexin 43 (Cx43), cardiac muscle α-actin (Actc1), and myosin heavy chain 6 (Myh6) were detected at different time points by immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and Western blot, and the proportions of beating cells at different time points were calculated. Results　The relative fluorescence intensity and mRNA and protein levels of α-MHC, α-actin, cTnT, Cx43, Actc1, and Myh6 in CFs in each group increased with increasing culture time (P<0.05), with significantly higher expression levels of myocardial-specific proteins at 14 days of culture than at 7 days (P<0.05). The relative fluorescence intensities and mRNA and protein levels of α-MHC, α-actin, cTnT, Cx43, Actc1, and Myh6 in CFs at 3, 7, 14, and 21 days of culture were significantly increased in the CTRP3-Lv group compared with the NC-Lv group (P<0.05), but were significantly decreased in CFs in the CTRP3-sh group compared with the NC-sh group (P<0.05). Beating cells appeared in CFs in each group at 7 days of culture. The proportion of beating cells in each group increased with increasing culture time (P<0.05), and the proportion was significantly higher at 14 days than at 7 days (P<0.05). The proportion of beating cells among CFs was increased in the CTRP3-Lv group at 7, 14, and 21 days of culture compared with the NC-Lv group (P<0.05), while the proportion of beating cells in the CTRP3-sh group was decreased compared with the NC-sh group (P<0.05). Conclusions　CTRP3 can enhance SeVGMT reprogramming of CFs into iCMs.

Abstract: Objective　To investigate the therapeutic effects of the newly developed phosphodiesterase 5 inhibitor, CPD1, on pathological myocardial hypertrophy induced by abdominal aortic constriction (AAC) in rats, and its impact on activation of the autophagy signaling pathway in myocardial tissue. Methods　Male Sprague Dawley rats weighing 180~200 g were divided randomly into five groups: Control, Sham, model (AAC), CPD1 treatment (AAC-CPD1,5 mg/kg), and sildenafil treatment (AAC-Sif, 20 mg/kg) groups. Rats in all groups except the Control group underwent blunt dissection of the abdominal aorta at the branch point of the left renal artery. Rats in the AAC and treatment groups also underwent constriction and ligation surgery, while rats in the Sham group underwent dissection without ligation. After 3 days of modeling, rats in the treatment groups received either CPD1 or sildenafil via gavage, while rats in the Control, Sham, and AAC groups received an equal volume of physiological saline by gavage, once daily for 8 weeks. Small-animal ultra-high-resolution echocardiography and left ventricular catheterization were employed to assess left heart function and the heart mass index, and expression levels of the hypertrophy indicator, atrial natriuretic peptide (ANP), the key autophagy pathway factor, p62, and LC3A/B in rat left heart tissue were evaluated by Western blot and reverse transcription-polymerase chain reaction. Results Abdominal aortic stenosis affected left heart function in rats, characterized by an increased cardiac mass index and significant enlargement of myocardial cell cross-sectional area. ANP expression levels in left heart tissue were significantly elevated (P<0.05), while autophagy signaling activity was reduced, with notable accumulation of LC3I protein and reduced conversion to LC3II. Expression levels of p62 protein were significantly increased. CPD1 and sildenafil significantly improved left ventricular function in AAC rats, reduced cardiac hypertrophy, inhibited expression levels of ANP and p62 proteins (P<0.05), activated autophagy signaling, and promoted the conversion of LC3I to LC3II. Notably, low-dose CPD1 treatment was equivalent to high-dose sildenafil. Conclusions　CPD1 promotes the activation of the autophagy signaling pathway in left heart tissue, inhibits the expression of p62 and ANP, reduces the cross-sectional area of myocardial cells, and improves pathological myocardial hypertrophy and left heart function impairment caused by AAC. CPD1 also has the advantage of a lower effective dose compared with sildenafil, offering a new treatment option for pathological myocardial hypertrophy.

Abstract: Objective　Investigating the effect and mechanism of resveratrol on cardiac function in exercise induced fatigue rats by regulating mitochondrial energy metabolism. Methods　Forty-eight healthy male Sprague Dawley rats (6~8 weeks old) were selected and divided randomly into a blank control (C) group, resveratrol administration (R) group, exercise-induced fatigue (E) group, and exercise-induced fatigue + resveratrol administration group (ER) (n=12 rats per group). Rats in the E and ER groups were subjected to weight-bearing 5% of their body weight for 60 minutes each day and exercise for 6 days per week for 6 weeks. Rats in the R and ER groups received resveratrol 50 mg/kg by gavage, 1 hour after exercise. The biochemical kit was used to detect the indicators of motor fatigue, myocardial injury and mitochondrial energy metabolism enzymes in rat myocardium. The mRNA expression levels of myocardial energy metabolism related regulatory factors were detected by real-time fluorescent quantitative PCR (RT-qPCR). Results　Plasma levels of blood urea nitrogen (BUN) and creatine kinase (CK) were significantly increased in rats in group E compared with group C (P<0.05, P<0.05), CK-MB and cTnI activity were also significantly increased (P<0.01, P<0.05), while activity levels of myocardial cytochrome C oxidase (COX) and succinate dehydrogenase (SDH) were significantly reduced (P<0.01, P<0.05). mRNA expression levels of the mitochondrial energy metabolism-related genes silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), and estrogen receptor-related receptor α (ERRα) were also significantly reduced (P<0.01, P<0.01, P<0.01). Serum levels of BUN and CK were significantly decreased in the ER group compared with group E (P<0.05, P<0.05), while CK-MB and cTnI activities were significantly decreased (P<0.05, P<0.05), myocardial COX and SDH activities were significantly increased (P<0.01, P<0.05), and SIRT1, PGC-1α and ERRα mRNA levels were also significantly increased (P<0.05, P<0.01, P<0.01). Conclusions　Resveratrol can effectively activate the sirtuin 1/peroxisome proliferator activated receptor γ coactivator 1α/estrogen-related receptor α signaling pathway, improve myocardial energy metabolism in exercise-fatigued rats, and protect against myocardial injury.

Abstract: Objective　To explore the effects and mechanism of calycosin-7-glucoside (CG) on lipopolysaccharide (LPS)-induced inflammatory injury in BV-2 cells and in a mouse model of neuroinflammation. Methods　An in vitro neuroinflammation model was induced by LPS stimulation of BV-2 cells. BV-2 cells were divided into blank (CON), model (LPS), dexamethasone (DEX), and low- and high-dose CG (CG 10 μmol/L, CG 20 μmol/L, respectively) groups. The cell viability in each group was detected by Cell Counting Kit-8 assay, interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels in the supernatant were detected by enzyme-linked immunosorbent assay (ELISA), and nitric oxide levels were detected using the Griess method. LPS was also used to induce neuroinflammation in mice in vivo. The mice were then divided randomly into blank (CON), model (LPS), aspirin, and low- and high-dose CG (CG 5 mg/kg, CG 10 mg/kg, respectively) groups. Pathological changes in the hippocampus were detected by hematoxylin/eosin staining. Serum levels of IL-6 and TNF-α were detected by ELISA, polarization of microglia was detected by immunofluorescence staining, and protein expression levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor κB (NF-κB, P65) and phosphorylated-NF-κB (p-P65) in the cortex were detected by Western blot. Results　CG alone or in combination with LPS in the concentration range of 2.5~160 μmol/L had no significant toxicity in BV-2 cells in vitro, compared with the CON group (P>0.05). IL-6, TNF-α, and NO levels in the cell supernatant were increased in the LPS group compared with the CON group (P<0.01), but were significantly reduced by CG (P<0.05, P<0.01). Hippocampal neurons were arranged loosely and disordered in the LPS group in vivo, compared with the CON group, and nuclear pyknosis was observed. Serum levels of IL-6 and TNF-α were increased (P<0.05, P<0.01). The number of ionized calcium binding adaptor molecule 1 (Iba1) /inducible nitric oxide synthase (iNOS) cells was increased (P<0.01), the number of CD206/Iba1 cells was decreased (P<0.01), and expression levels of TLR4, MyD88, and p-P65 protein in the cortex were increased (P<0.05). Compared with the LPS group, CG improved the pathological damage to the hippocampus and inhibited serum levels of IL-6 and TNF-α (P<0.01). CG also decreased the number of iNOS/Iba1 cells, increased the number of CD206/Iba1 cells (P<0.05,P<0.01), and significantly down-regulated TLR4, MyD88, and p-P65 protein levels in the cortex (P<0.05). Conclusions　CG can ameliorate neuroinflammation in mice by suppressing the TLR4/MyD88/NF-κB pathway.

Abstract: Objective　To explore the mechanism of Shanggan granules in suppressing pulmonary inflammation in mice infected with H1N1 influenza virus. Methods　A mouse model of pulmonary influenza virus infection was established by nasal inoculation with H1N1 influenza virus. Mice were divided into a normal control group, model group, positive control group, and low-, medium-, and high-dose Shanggan granules groups. Mice were treated for 7 days and then sacrificed, and the body weight and lung wet weight were measured. Pathological changes in the lung tissues were detected by hematoxylin/eosin (HE) staining. Tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, and transforming growth factor-β (TGF-β) levels in lung tissues were detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were detected using appropriate kits. Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) inflammatory signaling pathways were detected by real-time polymerase chain reaction, and TANK-binding kinase 1 (TBK1)/ interferon regulatory factor (IRF) signaling pathway proteins were detected by Western blot. Results　Both Shanggan granules and oseltamivir phosphate reduced the lung wet weight (P<0.05, P<0.001) in mice infected with influenza virus H1N1 compared with the model group, decreased the infiltration of inflammatory cells in lung tissue, reduced levels of the inflammatory factors TNF-α, IL-6, IL-8, and TGF-β (P<0.05, P<0.01, P<0.001), decreased levels of SOD and GSH-Px in lung tissue (P<0.05, P<0.01), and increased MDA levels (P<0.05, P<0.01). Shanggan granules and oseltamivir phosphate also reduced TLR4, MyD88, and p38 mRNA levels (P<0.05, P<0.01) and expression of TBK1/IRF3/7/NF-κB signaling pathway proteins (P<0.05, P<0.01, P<0.001). Conclusions Shanggan granules may effectively reduce lung injury, lung inflammation, and oxidative stress, via a mechanism related to the down-regulation of TLR4/NF-κB inflammatory signaling pathways.

Abstract: Objective　To determine the body weights and blood physiological and biochemical indicators in the Macaca mulatta brevicaudus(M.m.brevicaudus), to provide a reference for the breeding of experimental animals. Methods　A total of 180 wild M.m.brevicaudus (female and male) from the South Bay Macaque Reserve in Lingshui were selected as the research subjects. Body weights were measured using electronic scales and blood samples were collected. Routine blood indicators (red blood cell count, hemoglobin, white blood cell count, and platelet count) were detected using an automated blood cell analyzer, and biochemical indicators (alanine aminotransferase, aspartate aminotransferase, glucose, blood urea nitrogen) were measured using an automated biochemical analyzer. Data were analyzed using SPSS 18.0 software for descriptive statistics, and differences in body weights and blood indicators between sexes and age groups were compared using t-tests. Results　Adult male wild M.m. brevicaudus were significantly heavier than females (P<0.05); however, there were no significant differences in complete blood cell counts between female and male macaques (P>0.05). In terms of blood biochemical indicators, lactate dehydrogenase and total bilirubin levels differed significantly between female and male M.m.brevicaudus (P<0.05), but there were no significant differences in any other biochemical indicators. Conclusions This study established baseline data on the body weights and blood physiological and biochemical indicators of wild M.m. brevicaudus, providing a reference for their future breeding as experimental animals.

Abstract: Objective　To explore the influence of hsa_circ_0004535 on type 2 diabetes (T2DM) combined with metabolic-associated fatty liver disease (MAFLD) model mice. Methods　Forty-eight healthy SPF grade Balb/c mice were selected for modeling and divided into the following groups (n=6 per group): Control group: normal feed; T2DM group: diabetes model induced by high-glucose and high-fat diet; T2DM combined MAFLD group: non-alcoholic fatty liver high-glucose and high-fat diet-induced diabetes combined with fatty liver model; T2DM combined MAFLD+hsa_circ_NC group: after 4 weeks of modeling, 10 nmol hsa_circ_NC injected into the tail vein; T2DM combined MAFLD+hsa_circ_0004535 group: after 4 weeks of modeling, 10 nmol circ_0004535 injected into the tail vein; T2DM combined MAFLD+miRNA_NC group: after 4 weeks of modeling, 10 nmol miRNA blank control injected into the tail vein; T2DM combined MAFLD+miR-1827 agomir group: after 4 weeks of modeling, 10 nmol miR-1827 agomir injected into the tail vein; and T2DM combined MAFLD+miR-1827 antagomir group: after 4 weeks of modeling, 10 nmol miR-1827 antagomir injected into the tail vein. Mouse body weight was measured after the interventions and recorded weekly. Glucose and insulin tolerance tests were performed, blood lipids and liver function were measured, the liver and insulin resistance indexes were calculated, and pathological tests (hematoxylin/ eosin (HE), oil red O, and Masson staining, immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)) were performed to measure the degree of hepatic inflammation, fat deposition, and fibrosis. Results　(1)Body weight, liver weight, liver index, insulin resistance index, and biochemical indexes were all significantly lower in the hsa_circ_0004535 injection group compared with the hsa_circ_NC injection group and the T2DM combined MAFLD group (both P<0.05). (2)Steatosis vacuoles were reduced and smaller and inflammatory cell infiltration was reduced in the T2DM combined MAFLD+circ_0004535 group, as shown by HE and oil red staining. (3)TUNEL-positive cells were significantly reduced in the T2DM combined MAFLD+hsa_circ_0004535 group (P<0.05). (4)Collagen fiber deposition was significantly reduced in the T2DM combined MAFLD+hsa_circ_ 0004535 group, as shown by Masson staining (P<0.05). Conclusions　The expression of hsa_circ_0004535 and miRNA-1827 play important roles in regulating lipid metabolism, insulin sensitivity, inflammatory pathways, hepatocyte apoptosis, and hepatic fibrosis-related pathways in an animal model of T2DM combined with MAFLD.

Abstract: Objective　To investigate the effect of butorphanol on lipopolysaccharide-induced chondrocyte injury by regulating the stromal cell-derived factor-1α (SDF-1α)/C-X-C chemokine receptor 4 (CXCR4) pathway. Methods　Human C28/I2 chondrocytes were cultured in vitro and assigned to the following groups: control (normal culture), model (100 μmol/L lipopolysaccharide), model+low-dose butorphanol (100 μmol/L lipopolysaccharide+1 μmol/L butorphanol), model+medium-dose butorphanol (100 μmol/L lipopolysaccharide+2 μmol/L butorphanol), model+high-dose butorphanol (100 μmol/L lipopolysaccharide+4 μmol/L butorphanol), and model+high-dose butorphanol+NUCC-390 (100 μmol/L lipopolysaccharide+4 μmol/L butorphanol+500 nmol/L CXCR4 agonist NUCC-390). Cell viability, interleukin (IL) -6 and tumor necrosis factor-α (TNF-α) levels, apoptosis, and SDF1α/CXCR4 pathway-related proteins were evaluated by MTT assay, enzyme-linked immunosorbent assay, flow cytometry, and Western blot, respectively. Results　Chondrocyte survival rate and Bcl-2 protein expression were decreased while TNF-α, IL-6, apoptosis rate, Bax, Cleaved caspase-3, SDF-1α, and CXCR4 proteins were increased in the model group compared with the control group (P<0.05). The above indicators were improved in the model+low-, medium-, and high-dose butorphanol groups compared with the model group, while the result for the model+high-dose butorphanol+NUCC-390 group were opposite to those of the model+high-dose butorphanol group. Conclusions　Butorphanol may improve lipopolysaccharide-induced chondrocyte injury induced by inhibiting the SDF-1α/CXCR4 signaling pathway.

Abstract: Objective　To explore the method for grading the degree of uterine adhesion in a rat model. Methods　A rat model of uterine adhesion was established using the double-injury method. Paraffin sections were observed using HE staining and Masson staining to compare morphological changes in the uterus, endometrial thickness, gland and vessel counts, uterine cavity area, and adhesion severity. Rat sections were classified into three grades based on uterine cavity area for comparative analysis. Results　The average uterine cavity area and uterine cavity area/endometrial layer area were smaller in rats in the model group compared with the blank group (P<0.01). The uterine cavity area/endometrial layer area ratio was categorized into grades Ⅰ, Ⅱ, and Ⅲ, with a significant difference among the grades (P<0.05, P<0.01). Conclusions　The uterine cavity area/endometrial layer area ratio may reflect the grading difference in the degree of uterine adhesion in rats with uterine adhesions. This ratio may thus be used as a grading-evaluation criterion in the rat model of uterine adhesion, with implications for diagnostic grading in this model.

Abstract:Laboratory animal centers provide a crucial support platform for research and teaching in various disciplines in universities, including science, technology, agriculture, and medicine, providing a venue for animal experiments for faculty members and students. The facilities and equipment in these laboratory animal centers provide important safeguards to ensure the quality of animal housing environments and the health of personnel. This review summarizes the recent operation and maintenance of facilities and equipment and the management of troubleshooting at Yunnan University Laboratory Animal Center, with the aim of providing a comprehensive reference for enhancing the stability, reliability, efficiency, and energy conservation of equipment operation in university laboratory animal centers, and ensuring the safe and efficient operation of these centers.

Abstract:N7-methylguanosine (m⁷G) modification occurs at the 5’ cap of mRNA in eukaryotes, and is also found at specific sites on tRNA and rRNA, showing wide conservation across various biological organisms. Aberrant m⁷G modification is involved in the dysregulation of gene expression and serves as a biomarker for multiple cancers, with significant potential for applications in tumor diagnosis and therapy. This review summarizes the biological functions and regulatory mechanisms of m⁷G modification, and outlines its potential clinical applications. It also highlights the oncogenic roles of aberrant m⁷G modification and its association with prognosis, providing a detailed discussion of the role and molecular mechanisms of abnormal m⁷G modification in regulating drug resistance in various cancers.

Abstract:Sarcopenia is a systemic disease characterized by accelerated loss of skeletal muscle mass and function, leading to an increased incidence of adverse outcomes such as falls and fractures. Sarcopenia is classified into primary and secondary types, with primary sarcopenia being closely related to aging and posing a serious threat to a healthy life among the elderly. Sarcopenia has an insidious onset and is often overlooked in terms of its clinical treatment. Its pathogenesis is complex, involving functional changes and pathological alterations in multiple systems, and presenting major research challenges. Cell models can effectively be used to simulate the pathological changes of diseases under controllable conditions, thus facilitating the investigation of the etiology and factors influencing sarcopenia, and providing an important approach for in-depth studies of its mechanism; however, there is currently no standardized cell model in the field of sarcopenia research. Commonly used cell models currently include models involving protein metabolism interventions, oxidative stress, and inflammatory response interventions. This review considers the commonly used skeletal muscle cell types and modeling method of sarcopenia, to provide a solid foundation and important method ological reference for further simulation of the pathological process of sarcopenia in subsequent experimental studies.

Abstract:Vascular cognitive impairment (VCI) is a syndrome of cognitive decline attributed to vascular risk factors and cerebrovascular diseases. A range of pathophysiological processes induced by vascular injury, including inflammation, oxidative stress, cell death, disruption of the blood-brain barrier, and synaptic damage are intricately linked to the development of VCI. Nuclear factor E2-related factor 2 (Nrf2), encoded by the NFE2L2 gene, is a potent transcription factor that plays a critical role in antioxidant defense. Extensive research has demonstrated that Nrf2 mitigates oxidative stress and inflammation by upregulating the expression of antioxidant response elements, thereby reducing the production of reactive oxygen species. Nrf2 also modulates programmed cell death, enhances blood-brain barrier integrity, and promotes synaptic plasticity, ultimately delaying the progression of VCI. This review examines the role of Nrf2 in VCI and highlights recent research on traditional Chinese medicines targeting Nrf2 for the prevention and treatment of VCI, thus providing novel insights and approaches for managing this condition.

Abstract:Multiple sclerosis (MS) is a complex autoimmune disorder characterized by inflammatory demyelination in the central nervous system. Prominent symptoms include damage to myelin sheaths in the brain, optic nerve, and spinal cord, as well as axonal dysfunction; however, the exact causes and mechanisms of MS remain unclear. Genetic and environmental factors are thought to interact via autoimmune mechanisms, potentially triggering the disease. Recent studies suggest that abnormal activation of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome may play a critical role in the pathogenesis of MS. In this context, this review summarizes the molecular mechanisms underlying NLRP3 activation and its connection to MS, considering relevant literature from the past decade. The findings aim to provide insights into the progression of MS and to identify potential therapeutic strategies by elucidating the underlying mechanisms.

Abstract:The relationship between the pathogenesis of cardiovascular diseases in individuals and maternal obesity (MO) has attracted much recent attention. In addition to jeopardizing maternal health, MO increases the heart-attack risk in the offspring by affecting the development of the cardiovascular system. High prenatal calorie intake leads to fetal overnutrition, which affects the use of fatty acids, glucose, and ketones in cardiomyocytes. MO has been shown to affect the offspring via cardiomyocyte metabolism and remodeling, as well as increasing reactive oxygen species in the heart, thereby stimulating the mammalian target of rapamycin and Hippo pathways to induce cardiomyocyte proliferation and hypertrophy. Notably, the Hippo pathway could represent a potential therapeutic target for cardiomyocyte hypertrophy. This review considers the role of MO in regulating fetal cardiomyocyte metabolism and hypertrophy in the offspring, and the related epigenetic mechanism. We also discuss the long-term effects of MO on offspring cardiomyocyte health. The findings suggest that metabolic memory, cross-generational genetic effects, and early-life interventions may be important avenues for future research.