Incidence Of Acute Kidney Injury In Mild, Moderate And Severe Cases Of Coronavirus Disease DOI Creative Commons

Mahvesh Mahmud,

Ashok Kumar,

Khurram Baqai

et al.

Journal of Rawalpindi Medical College, Journal Year: 2023, Volume and Issue: 27(4)

Published: Dec. 30, 2023

Objective: The purpose of this research was to determine the incidence Acute Kidney Injury (AKI) in COVID-19-affected patients Methods: This retrospective cohort study conducted at Ziauddin Hospital Clifton Campus from June December 2020. Adult with AKI or acute-on-chronic kidney disease (ACKD) were included a study. Patients infected SARS-CoV2 and renal involvement directed towards ICU/Nephrology departments which have expertise perform laboratory analysis, radiography institution treatment. Supplemental oxygen use documented. also assessed information about therapy (antivirals, immunomodulators, RRT) results (renal function recovery death). Results: After excluding obstructive AKI, total 180 (mean age 50.1 years) 104 males 76 females research. 120 found prerenal, 60 had intrinsic significant differences between mild, moderate, severe cases (p=0.004). injury survivors complete rate 70%, partial 22%, hemodialysis dependency 8%. Conclusion: COVID-19 infection often develop more those critical stages exhibit proteinuria dipstick hematuria. Long-term follow-up for should be done evaluate its influence on outcome, larger samples are required elucidate association damage. Keywords: Coronavirus Disease, Renal Replacement Therapy, proteinuria, hematuria

Language: Английский

Beyond the virus: ecotoxicological and reproductive impacts of SARS-CoV-2 lysate protein in C57Bl/6j female mice DOI
Bárbara Beatriz da Silva Nunes,

Juliana dos Santos Mendonça,

Letícia Paiva de Matos

et al.

Environmental Science and Pollution Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 2, 2025

Language: Английский

Citations

0
Incidence, pathophysiology, risk factors, histopathology, and outcomes of COVID-19-induced acute kidney injury: a narrative review DOI
Abdelhamid Hachimi, Bilal El‐Mansoury, Mohamed Merzouki

et al.

Microbial Pathogenesis, Journal Year: 2025, Volume and Issue: unknown, P. 107360 - 107360

Published: Jan. 1, 2025

Language: Английский

Citations

0
Insights into the Correlation and Immune Crosstalk Between COVID-19 and Sjögren’s Syndrome Keratoconjunctivitis Sicca via Weighted Gene Coexpression Network Analysis and Machine Learning DOI Creative Commons
Yaqi Cheng, Liang Zhao, Huan Yu

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(3), P. 579 - 579

Published: Feb. 25, 2025

Background: Although autoimmune complications of COVID-19 have aroused concerns, there is no consensus on its ocular complications. Sjögren’s syndrome an disease accompanied by the abnormality keratoconjunctivitis sicca (SS-KCS), which may be influenced COVID-19. Thereby, we explored possible interaction between and SS-KCS, aimed to elucidate potential correlated mechanism. Methods: Differentially expressed genes (DEGs) in SS-KCS transcriptome data obtained from gene expression omnibus database were identified, COVID-19-related screened using weighted coexpression network analysis. Common verified four machine-learning diagnostic predictors. The clinical relationship two common hub was analyzed. Finally, immune cell types infiltrating microenvironment dataset analyzed CIBERSORT, interrelation key differentially cells via Pearson correlation. Results: Ten primary mRNAs intersecting DEGs, WGCNA genes. After a multifaceted evaluation mainstream predictors, most accurate sensitive random forest model identified CR1 TAP2 as SS-KCS. Together with information COVID-19, significantly status severity positively M0 M2 macrophages, neutrophils, CD4+ memory resting T negatively activated NK cells, monocytes, CD8+ cells. Conclusions: We validated associated both investigated mechanisms underlying their interaction, help early prediction, identification, diagnosis, management SARS-CoV-2 infection-related or many other immune-related long COVID period.

Language: Английский

Citations

0
Reversible and irreversible inhibitors of coronavirus Nsp15 endoribonuclease DOI Creative Commons
Jerry Chen, Rabih Abou Farraj, Daniel Limonta

et al.

Journal of Biological Chemistry, Journal Year: 2023, Volume and Issue: 299(11), P. 105341 - 105341

Published: Oct. 12, 2023

The emergence of severe acute respiratory syndrome coronavirus 2, the causative agent disease 2019, has resulted in largest pandemic recent history. Current therapeutic strategies to mitigate this have focused on development vaccines and drugs that inhibit viral 3CL protease or RNA-dependent RNA polymerase enzymes. A less-explored potentially complementary drug target is Nsp15, a uracil-specific endonuclease shields coronaviruses other nidoviruses from mammalian innate immune defenses. Here, we perform high-throughput screen over 100,000 small molecules identify Nsp15 inhibitors. We characterize potency, mechanism, selectivity, predicted binding mode five lead compounds. show one these, IPA-3, an irreversible inhibitor might act via covalent modification Cys residues within Nsp15. Moreover, demonstrate three these inhibitors (hexachlorophene, CID5675221) block 2 replication cells at subtoxic doses. This study provides pipeline for identification pinpoints compounds further against 2019 related infections.

Language: Английский

Citations

8
Targeting macrophagic RasGRP1 with catechin hydrate ameliorates sepsis-induced multiorgan dysfunction DOI Creative Commons
Zhixi Li,

Yongjing Yu,

Yue Bu

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 130, P. 155733 - 155733

Published: May 12, 2024

The proinflammatory response induced by macrophages plays a crucial role in the development of sepsis and resulting multiorgan dysfunction. Identifying new regulatory targets for macrophage homeostasis devising effective treatment strategies remains significant challenge contemporary research. This study aims to identify develop treating sepsis. Macrophage infiltration septic patients lungs, kidneys, brains caecum ligation puncture (CLP)-induced mice was observed using CIBERSORT immunofluorescence (IF). Upon integrating MSigDB database GSE65682 dataset, differently expressed macrophage-associated genes (DEMAGs) were identified. Critical DEMAGs confirmed through machine learning. protein level critical DEMAG detected PBMCs patients, RAW264.7 cells, ELISA, western blot, immunohistochemistry, IF. siRNA applied investigate effect cells. A natural product library screened find compound targeting protein. binding compounds proteins analyzed molecular docking, dynamics simulations, CETSA, MST analysis. therapeutic efficacy against then evaluated vitro vivo experiments. inversely correlated with survival patients. differentially molecule RasGRP1 frequently LPS-induced mice. Silencing alleviated oxidative stress LPS-treated Catechin Hydrate (CH) identified as an inhibitor RasGRP1, capable maintaining mitigating lung, kidney, brain damage during demonstrates that novel activator responses, excessive inflammation associated CH shows potential inhibiting RasGRP1.

Language: Английский

Citations

3
Potential Alternative Receptors for SARS-CoV-2-Induced Kidney Damage: TLR-4, KIM-1/TIM-1, and CD147 DOI Creative Commons
Nada J. Habeichi, Ghadir Amin,

Bachir Lakkis

et al.

Frontiers in Bioscience-Landmark, Journal Year: 2024, Volume and Issue: 29(1), P. 8 - 8

Published: Jan. 12, 2024

Kidney damage in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can occur even patients with no underlying kidney disease. Signs of problems progress to a state that demands dialysis and hampering recovery. Although not without controversy, emerging evidence implicates direct infectivity SARS-CoV-2 the kidney. At early stage pandemic, consideration was mainly on well-recognized angiotensin-converting enzyme (ACE2) receptor as being site for viral interaction subsequent cellular internalization. Despite abundance ACE2 receptors kidneys, researchers have expanded beyond identified novel entry pathways could be advantageously explored therapeutic targets. This review presents potential involvement toll-like 4 (TLR-4), injury molecule-1/T cell immunoglobulin mucin domain 1 (KIM-1/TIM-1), cluster differentiation 147 (CD147) SARS-CoV-2-associated renal damage. In this context, we address unresolved issues surrounding infectivity.

Language: Английский

Citations

2
Freshwater Pollution by Sars-Cov-2 Lysate Protein Induces Multiple Impacts on C57bl/6j Female Mice DOI
Bárbara Beatriz da Silva Nunes,

Juliana dos Santos Mendonça,

Letícia Paiva de Matos

et al.

Published: Jan. 1, 2024

Download This Paper Open PDF in Browser Add to My Library Share: Permalink Using these links will ensure access this page indefinitely Copy URL DOI

Language: Английский

Citations

0
IGF-II Regulates Lysyl Oxidase Propeptide and Mediates its Effects in part via Basic Helix-Loop-Helix E40 DOI
Adegboyega Timothy Adewale, Shailza Sharma, Joe E. Mouawad

et al.

Matrix Biology, Journal Year: 2024, Volume and Issue: 132, P. 24 - 33

Published: June 7, 2024

Language: Английский

Citations

0
Long COVID: A Molecular, Cellular and Histopathology Overview DOI Open Access
Bárbara Rafaela da Silva Barros,

Leonardo Carvalho de Oliveira Cruz,

Georon Ferreira de Sousa

et al.

Journal of Biosciences and Medicines, Journal Year: 2023, Volume and Issue: 11(09), P. 90 - 113

Published: Jan. 1, 2023

Long COVID has been studied as different sequelae that some individuals can develop after the acute phase of disease. Persistent symptoms such dry cough, fatigue, and dyspnea remain six months COVID-19 cure. Others lung fibrosis, kidney injury, thrombotic risk also are observed. Here, a deep review each human organ system infected by virus was performed aiming to show how molecules expression cell signaling induce organism cure or injuries and, subsequently sequelae. The suggests importance public health surveillance for these cases including more comprehensive analysis molecular biology tools clarify assist in prognosis, treatment, preventive methods potentially serious disorders post-COVID-19 patients.

Language: Английский

Citations

0
Mechanism of transforming growth factor-<bold>β</bold>1 induce renal fibrosis based on transcriptome sequencing analysis DOI
Huanan Li,

Peifen Li,

Shanyi Li

et al.

Journal of Zhejiang University (Medical Sciences), Journal Year: 2023, Volume and Issue: 52(5), P. 594 - 604

Published: Sept. 28, 2023

To explore the mechanism of transforming growth factor-β1 (TGF-β1) induce renal fibrosis.Renal fibroblast NRK-49F cells treated with and without TGF-β1 were subjected to RNA-seq analysis. DESeq2 was used for Differentially expressed genes screened criteria false discovery rate<0.05 l o g 2 F C >1. Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analyses performed differentially genes. encoding transcription factors further differential expression Then, these during fibrosis verified using unilateral ureteral obstruction (UUO)-induced mouse model a public gene dataset (GSE104954).After treatment 6, 12 24 h, 552, 1209 1028 identified, respectively. GO analysis indicated that significantly enriched in development, cell death, migration. KEGG showed early stage induction (TGF-β1 6 h), changes Hippo, TGF-β Wnt signaling pathways observed, while late extracellular matrix-receptor interaction, focal adhesion adherens junction mainly enriched. Among 291 up-regulated 13 (Snai1, Irf8, Bhlhe40, Junb, Arid5a, Vdr, Lef1, Ahr, Foxo1, Myc, Tcf7, Foxc2, Glis1) encoded factors. Validation induced 9 (encoded by Snai1, Tcf7), levels other 4 did not change after treatment. results UUO-induced Myc Tcf7 UUO, Vdr down-regulated there no significant Lef1. based on GSE104954 IRF8 overexpressed tubulointerstitium patients diabetic nephropathy or IgA nephropathy, MYC highly expressions 7 different compared control group.TGF-β1 induces fibroblasts, among which Irf8 identified as potential targets chronic kidney disease fibrosis.目的: 探究转化生长因子-β1（TGF-β1）诱导肾纤维化的机制。方法: 将TGF-β1处理和未处理的肾成纤维细胞NRK-49F进行转录组测序，采用DESeq2分析测序结果，以错误发现率低于0.05且log2FC绝对值大于1为标准筛选差异表达的基因，并对差异表达的基因进行基因本体（GO）、京都基因和基因组百科全书（KEGG）通路富集分析。进一步筛选差异表达基因中编码转录因子的基因，并利用单侧输尿管梗阻诱导的小鼠肾纤维化模型和高通量基因表达数据库GSE104954数据集对这些基因在肾纤维化过程中的表达进行验证。结果: TGF-β1处理6、12和24 h后，分别有552、1209和1028个差异表达基因。GO分析表明，这些差异表达基因在发育、细胞死亡和细胞迁移过程中显著富集。KEGG分析显示，在TGF-β1诱导早期（TGF-β1处理6 h）主要表现为Hippo、TGF-β、Wnt信号通路的变化，而在TGF-β1诱导晚期（TGF-β1处理24 h）主要表现为细胞外基质受体相互作用、局灶黏附和黏附分子连接等相关通路的改变。在TGF-β1处理6 h时291个上调的差异表达基因中，Snai1、Irf8、Bhlhe40、Junb、Arid5a、Vdr、Lef1、Ahr、Foxo1、Myc、Tcf7、Foxc2、Glis1等13个基因编码转录因子。在细胞模型中验证发现，TGF-β1可以诱导其中9个编码转录因子基因（Snai1、Irf8、Bhlhe40、Junb、Arid5a、Vdr、Lef1、Myc、Tcf7）的表达，其余4个基因的表达水平在TGF-β1处理后无显著变化。在动物模型验证中发现，Snai1、Irf8、Bhlhe40、Junb、Arid5a、Myc和Tcf7显著上调，而Vdr显著下调，Lef1无显著变化。在GSE104954数据集中验证发现，IRF8在糖尿病肾病患者和IgA肾病患者的肾小管间质中显著高表达，MYC在糖尿病肾病患者中高表达，而其他7个基因的表达产物与对照组相似。结论: TGF-β1诱导肾成纤维细胞基因差异表达，Irf8和Myc可能是慢性肾脏病和肾纤维化的潜在靶点。.

Language: Английский

Citations

0