Histology and histopathology最新文献

{"title":"Melatonin protects against sarcopenia in middle-aged mice.","authors":"Fei Fang, Ping Yu, Xiaoying Sun, Zhixing Shen, Fan Zhang, Jianwei Sun","doi":"10.14670/HH-18-814","DOIUrl":"10.14670/HH-18-814","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a common age-related disease. Melatonin (MEL) is an age-related endocrine hormone, which displays a crucial role in resisting oxidative stress during aging. Importantly, the antioxidant properties of MEL can be mediated by mitochondria.</p><p><strong>Objective: </strong>Therefore, we wondered whether MEL could mitigate oxidative stress caused by mitochondria in sarcopenia.</p><p><strong>Methods: </strong>The middle-aged mice were administered 5 mg/kg/d and 10 mg/kg/d of MEL for 2 months. Young mice were used as the control group.</p><p><strong>Results: </strong>After treatment with MEL, the grip strength of the fore/hind limbs, running time, and distance were elevated, and the weights of the gastrocnemius (GA), tibialis anterior (TA), extensor digitorum longus (EDL), and soleus (SOL) were enhanced in middle-aged mice. Additionally, MEL was observed to alleviate histological damage and increase the cross-sectional area of muscle fibers in GA tissues of middle-aged mice. Furthermore, following MEL treatment, there was an increase in the percentage and size of normal mitochondria as well as mtDNA copy number but a reduction in the levels of malondialdehyde (MDA), protein carbonyl, and reactive oxygen species (ROS) in the GA tissues of middle-aged mice. At the molecular level, MEL repressed the levels of ATROGIN-1, muscle RING-finger protein-1 (MURF-1), and the ratio of p-P38/P38, but elevated the expression of cytochrome c oxidase subunit 4 (COX4), cystatin C (CYTC), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (TFAM), and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in the GA tissues of middle-aged mice. Importantly, 10 mg/kg MEL was more efficacious in the treatment of sarcopenia than 5 mg/kg MEL.</p><p><strong>Conclusion: </strong>MEL attenuates sarcopenia in middle-aged mice, and the mechanism may relate to mitochondria-induced oxidative stress and the PGC-1α/TFAM pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"745-755"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-gated inwardly rectifying K⁺ (GIRK/K_ir3) channels: Molecular, cellular, and subcellular diversity.","authors":"Alejandro Martín-Belmonte, Carolina Aguado, Rocio Alfaro-Ruíz, Rafael Luján","doi":"10.14670/HH-18-822","DOIUrl":"10.14670/HH-18-822","url":null,"abstract":"<p><p>G protein-gated inwardly rectifying K⁺ (GIRK/K_ir3) channels are mainly expressed in excitable cells such as neurons and atrial myocytes, where they can respond to a wide variety of neurotransmitters. Four GIRK subunits have been found in mammals (GIRK1-4) and act as downstream targets for various Gαi/o-linked G protein-coupled receptors (GPCRs). Activation of GIRK channels produces a postsynaptic efflux of potassium from the cell, responsible for hyperpolarization/inhibition of the neuron. A growing body of evidence suggests that dysregulation of GIRK signalling can lead to excessive or deficient neuronal excitability, which contributes to neurological diseases and disorders. Therefore, GIRK channels are proposed as new pharmacological targets. The function of GIRK channels in neurons is not only determined by their biophysical properties but also by their cellular and subcellular localization patterns and densities on the neuronal surface. GIRK channels can be located within several subcellular compartments, where they have many different functional implications. This subcellular localization changes dynamically along the neuronal surface in response to drug intake. Ongoing research is focusing on determining the proteins that form macromolecular complexes with GIRK channels and are responsible for fast and precise signalling under physiological conditions, and how their alteration is implicated in pathological conditions. In this review, the distinct regional, cellular, and subcellular distribution of GIRK channel subunits in the brain will be discussed in view of their possible functional and pathological implications.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"597-620"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRIP1 is a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction.","authors":"Wanliu Zhang, Jingqian Lu, Yan Gao, Qianhong Song, Shihua Luo, Yi Li","doi":"10.14670/HH-18-820","DOIUrl":"10.14670/HH-18-820","url":null,"abstract":"<p><strong>Background and objective: </strong>From a clinical standpoint, myocardial ischemia/reperfusion injury (MIRI) has always been an enormous challenge for the treatment of acute myocardial infarction (AMI). Molecular targeting therapy may help overcome this challenge. The present work aimed to elucidate the possible involvement of Yin-Yang 1 (YY1)/nuclear receptor-interacting protein 1 (NRIP1) and discover the molecular mechanism of MIRI.</p><p><strong>Methods: </strong>Herein, a cardiomyocyte ischemia/reperfusion (I/R) model was established via oxygen-glucose deprivation/re-oxygenation (OGD/R) damage in H9c2 cardiomyocytes. Reverse transcription-quantitative PCR and western blotting were conducted to measure the levels of YY1 and NRIP1 at the RNA and protein levels, respectively. H9c2 cell viability and apoptosis were assayed using the Cell Counting Kit-8, flow cytometry, and western blotting. In addition, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels were analyzed as markers of oxidative stress. Additionally, mitochondrial membrane potential, which was measured via JC-1 staining, ATP content, Complex I activity, mitochondrial DNA copy number, and mitochondrial permeability transition pore (mPTP) opening rate were analyzed to evaluate mitochondrial activity. Moreover, luciferase reporter and chromatin immunoprecipitation assays experimentally validated the predicted affinity of YY1 with the NRIP1 promoter according to the HumanTFDB online tool.</p><p><strong>Results: </strong>YY1/NRIP1 were both highly expressed in OGD/R-injured H9c2 cardiomyocytes. Downregulation of NRIP1 improved cell viability, whereas it inhibited cell apoptosis and oxidative stress, and suppressed mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes. Importantly, it was verified that YY1 could bind to the NRIP1 promoter to positively regulate NRIP1 expression. The protective effects of NRIP1 knockdown against cardiomyocyte damage and mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes were partly abolished through overexpression of YY1.</p><p><strong>Conclusion: </strong>NRIP1 emerged as a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction, providing novel ideas for targeted treatments to alleviate MIRI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"773-784"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress on three-dimensional visualizing skin architecture with multiple immunofluorescence staining and tissue-clearing approaches.","authors":"Yuqing Wang, Wanzhu Bai, Xiaoyu Wang","doi":"10.14670/HH-18-815","DOIUrl":"10.14670/HH-18-815","url":null,"abstract":"<p><p>The skin forms the external covering of the body and is its largest organ, comprising many different cell types. Although the diversity of these cells has been widely studied with various histological methods, our understanding of skin architecture is mainly established on thin tissue sections, which restricted the information available to two dimensions. The development of innovative techniques to induce optical transparency (\"clearing\") in biological tissues has enabled researchers to visualize the three-dimensional reconstruction of intact organs and thick tissue sections at a cellular resolution. With the aid of tissue-clearing treatment, the labeled cutaneous nerve fibers and blood vessels can be followed for a longer distance on the thicker skin section or the whole mount skin under a fluorescence microscopy or a confocal microscopy. It is beneficial for demonstrating the morphological characteristics of nerve fibers and blood vessels themselves, as well as their spatial interconnection. In this review, we provide a brief summary of the literature on the use of tissue optical clearing methods and describe our experience of multiple fluorescent staining and tissue clearing approaches on thicker skin sections and whole-mount skin in our laboratory. Given the existing conventional methods, we expected to provide a more effective approach to comprehensively study skin architecture.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"645-651"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrahydropalmatine promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate atherosclerosis.","authors":"Hui Wang, Ke Ding, Jiaqi He, Jiahong Wang","doi":"10.14670/HH-18-809","DOIUrl":"10.14670/HH-18-809","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) is a chronic progressive arterial disease that is associated with macrophage autophagy and AMP-activated protein kinase (AMPK)/mechanistic target of the rapamycin (mTOR) pathway. Tetrahydropalmatine (THP) can activate AMPK-dependent autophagy. We aim to study the mechanism of macrophage autophagy mediated by THP in the treatment of AS via the AMPK/mTOR pathway.</p><p><strong>Methods: </strong>High-fat diet apolipoprotein E-deficient mice and ox-LDL-induced RAW264.7 cells were used to mimic the AS model, then THP was administered. Cell viability was detected by MTT. Pathological aorta lesions were detected using Hematoxylin and Eosin, Masson, and oil red staining. Lipid metabolism indices and inflammatory factors were measured using ELISA. A transmission electron microscope was used to observe autophagosomes. Autophagy and AMPK/mTOR pathway protein expression was detected by immunofluorescence and Western blot. The AMPK inhibitor 9-β-d-Arabinofuranosyl Adenine (Ara-A) was used to validate the effect of THP. The mRNA expression of <i>Beclin-1</i> and <i>MCP-1</i> was detected by q-PCR.</p><p><strong>Results: </strong>THP administration regulated lipid metabolism by lowering total cholesterol, triacylglycerol, low-density lipoprotein, and high-density lipoprotein levels, and suppressed aortic damage. THP suppressed aortic damage and regulated lipid metabolism by altering serum lipid levels. THP reduced inflammation and macrophage CD68 expression. Twenty μg/mL THP reduced cell viability. THP decreased cholesterol uptake and increased efflux, promoting autophagy. THP increased autophagosome number, LC3B expression, and autophagy markers p-AMPK/AMPK and LC3-II/LC3-I. THP also decreased p-mTOR/mTOR and P62. THP increased <i>Beclin-1</i> mRNA expression and decreased <i>MCP-1</i> mRNA expression. Ara-A reversed THP's effects.</p><p><strong>Conclusion: </strong>THP promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate AS.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"697-710"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of morphology, apoptosis, and cell proliferation of the uterus in postmenopausal women.","authors":"Weronika Ratajczak, Malwina Łazowska, Maria Laszczyńska, Aleksandra Rył, Anna Lubkowska, Małgorzta Zimny, Andrzej Kram, Olimpia Sipak","doi":"10.14670/HH-18-819","DOIUrl":"10.14670/HH-18-819","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study was to evaluate the morphology (atrophy and fibrosis), apopto-sis, and cell proliferation in the uterine wall. The research material came from postmenopausal women who had undergone hysterectomy due to uterine myomas or prolapse of the reproductive organ and were not taking menopausal hormone therapy (MTH).</p><p><strong>Material and methods: </strong>The collected material was divided into three groups. Group I (n=18) con-sisted of uterine sections taken 1 to 5 years after the last menstruation, Group II (n=17) 6 to 10 years after the last menstruation, and Group III (n=15) over 11 years after the last menstruation. To assess morphology and fibrosis, the uterine sections were subjected to hematoxylin and eosin (HE) staining and to Mallory's staining. In addition, we performed a histochemical examination to identify apopto-sis in endometrial and myometrial cells using the TUNEL method. An immunohistochemical analysis of endometrial and myometrial cells was also performed to detect the location of the proliferating cell nuclear antigen (PCNA).</p><p><strong>Results: </strong>Differences in apoptosis were only found in the myometrium between Group I and Group III, and were strongest in Group I myometrial cells, and weakest in Group III. Neither the endome-trium nor the myometrium showed statistically significant differences in the overall percentage of PCNA(+) cells between groups.</p><p><strong>Conclusion: </strong>Morphological changes in the endometrial and myometrial layers of postmenopausal uteri increased with time since the last menstruation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"653-667"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR-mediated WNK4 point mutation aggravates tumor progression and weakens chemotherapy sensitivity in gastric cancer.","authors":"Xiaojun Ying, Zhen Ying, Xiaobing Gao, Yong Wang, Xinting Lv","doi":"10.14670/HH-18-810","DOIUrl":"10.14670/HH-18-810","url":null,"abstract":"<p><strong>Objective: </strong>Gastric cancer (GC) is the fifth most common malignancy, the molecular targets of which have been increasingly explored in recent years. As a serine/threonine protein kinase, the role of WNK lysine deficient protein kinase 4 (WNK4) in GC was clarified in this study.</p><p><strong>Methods: </strong>Human GC lines AGS and MKN45 were stably transfected with a WNK4 mutant constructed by the CRISPR/Cas9 method and treated with cis-dichlorodiammine platinum (CDDP, 2 μg/mL) and 5-fluorouracil (5-FU, 5 μg/mL) for 48h. Tumor-bearing mice were established with 5×10⁶ mutant-type AGS cells, and injected with 40 mg/kg WP1066, the inhibitor of signal transducer and activator of transcription 3 (STAT3), for 21 days. Cell malignant potential and tumor growth were assessed. STAT3 activation was identified by western blot and immunohistochemistry. The interaction between WNK4 and STAT3 was determined using co-immunoprecipitation and immunofluorescence co-localization.</p><p><strong>Results: </strong>WNK4 mutation promoted proliferation and invasion, and upregulated the p-STAT3/STAT3 value in GC cells with/without 5-FU and CDDP treatments, while inhibiting apoptosis of GC cells without drug treatment. In tumor-bearing mice, WNK4 mutation accelerated tumor growth, increased levels of p-STAT3, STAT3, and p-STAT3/STAT3, and strengthened the co-immunoprecipitation and co-localizing with STAT3; however, these effects were reversed by WP1066 treatment.</p><p><strong>Conclusion: </strong>Through activating STAT3, WNK4 mutation impacts both the natural and drug-treated growth of GC cells or tumors, suggesting a new avenue for preclinical research.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"711-720"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effectiveness of edible bird's nest in lowering VEGF, CD31, and PDGFR-β levels in diabetic retinopathy in rats with type 1 diabetes.","authors":"Manaras Komolkriengkrai, Udomlak Matsathit, Nualpun Sirinupong, Wipapan Khimmaktong","doi":"10.14670/HH-18-825","DOIUrl":"10.14670/HH-18-825","url":null,"abstract":"<p><strong>Aims: </strong>Diabetic eye disease, known as diabetic retinopathy (DR), is one of the problems that can arise from having high blood sugar for an extended period. This study aimed to investigate the effect of the edible bird's nest (EBN) on retinal angiogenesis in diabetic rats.</p><p><strong>Methods: </strong>The 50 rats were separated into five different groups, each containing 10 rats: control, diabetes (DM), bird's nest-fed diabetes (75 mg/kg Body weight; BW), (EBN 75), (150 mg/kg BW) (EBN 150), and glyburide (GR) for an eight-week study. H&E and Masson's trichrome staining were utilized to investigate the retinal tissue and vascular changes. The immunofluorescence study was used to detect angiogenic protein expression. The vascular corrosion cast/SEM method was also used to evaluate capillary plexus formation within the retinal layer.</p><p><strong>Results: </strong>From histological studies, DM rats have thinning of the retinal layer. Remarkably, the retinal vessels displayed dilations resembling ruptured blood vessels. The expression of vascular endothelial growth factor (VEGF) (30.51±2.62), cluster of differentiation 31 (CD31) (28.18±0.22), and platelet-derived growth factor receptor beta (PDGFR-β) (141.67±0.97) were increased. EBN 75 exhibited some small improvements in their blood vessels and eye tissue. At a dose of 150 mg/kg BW, EBN proved to be more effective. There was a significant decrease in VEGF and CD31 expression compared with the diabetic group (<i>p</i><0.001 and <i>p</i><0.01, respectively).</p><p><strong>Conclusions: </strong>These studies have demonstrated that EBN can lower the growth levels of VEGF, CD31, and PDGFR-β, which results in a decrease in angiogenesis and a recovery from a variety of diabetic retinopathy-related diseases.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"669-678"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of KMT2D-mediated epigenetic modification in IL-1β-induced nucleus pulposus cell degeneration.","authors":"Hongjiang Liu, Haiquan Liu, Zuyu Meng, Wensheng Zhang","doi":"10.14670/HH-18-813","DOIUrl":"10.14670/HH-18-813","url":null,"abstract":"<p><strong>Background: </strong>Intervertebral disc (IVD) degeneration (IVDD) is characterized by structural destruction accompanied by accelerated signs of aging. This study aimed to investigate the mechanism of lysine methyltransferase 2D (KMT2D) in the proliferation, apoptosis, and inflammation of nucleus pulposus cells (NPCs) in IVDD.</p><p><strong>Methods: </strong>Mouse-derived NPCs were cultured and induced with interleukin-1 beta (IL-1β) to establish cell models. KMT2D expression was detected by western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). KMT2D expression was interfered with, and the contents of IL-18, IL-6, and tumor necrosis factor (TNF) were detected by enzyme-linked immunosorbent assay. Cell proliferation, apoptosis, and the expression of miR-133a-5p and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2) were measured. The enrichment of KMT2D and Histone 3 Lysine 4 monomethylation/dimethylation (H3K4me1/2) on the miR-133a-5p promoter was analyzed by chromatin immunoprecipitation and qPCR. The binding of miR-133a-5p and PFKFB2 was analyzed by a dual-luciferase assay.</p><p><strong>Results: </strong>IL-1β treatment promoted KMT2D expression in NPCs. KMT2D knockdown reduced inflammation and apoptosis and promoted the proliferation of IL-1β-induced NPCs. Mechanistically, KMT2D upregulated miR-133a-5p expression by increasing the level of H3K4me2 at the miR-133a-5p promoter, thereby promoting the binding between miR-133a-5p and PFKFB2 and downregulating the transcription of PFKFB2. miR-133a-5p overexpression or PFKFB2 knockdown alleviated the protective effect of KMT2D knockdown on IL-1β-induced NPCs.</p><p><strong>Conclusion: </strong>KMT2D promoted miR-133a-5p expression through H3K4me2 methylation, thereby promoting the binding of miR-133a-5p to PFKFB2, reducing the mRNA level of PFKFB2, promoting inflammation and apoptosis of IL-1β-induced NPCs, and inhibiting NPC proliferation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"733-743"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent insights into limb-girdle muscular dystrophy: Impacts, therapy, and challenges.","authors":"Chen-Chen Sun, Jiang-Ling Xiao, Zhe Zhao, Heng-Yuan Liu, Chang-Fa Tang","doi":"10.14670/HH-18-929","DOIUrl":"https://doi.org/10.14670/HH-18-929","url":null,"abstract":"<p><p>Limb-girdle muscular dystrophy (LGMD) is a genetically heterogeneous group of muscle disorders characterized by progressive muscle atrophy and loss of motor function. Over 30 subtypes have been identified and classified into two main inheritance patterns: autosomal dominant and autosomal recessive. Besides primarily affecting skeletal muscle, certain subtypes also impact the cardiac and respiratory muscles, significantly influencing disease progression and patient survival. Substantial progress has been made in understanding the pathogenic genes and molecular mechanisms of LGMD; however, developing disease-modifying therapies remains challenging due to genetic heterogeneity, limitations in gene delivery technologies, and secondary pathological complications. Current treatments are primarily supportive, focusing on symptom management and improving quality of life rather than addressing the underlying cause. This paper summarizes recent advances in LGMD pathogenesis and emerging therapeutic strategies, highlighting progress and remaining challenges in the field.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18929"},"PeriodicalIF":2.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}