A5022950257- Mitochondrial Function and Pathology
- Genetics, Aging, and Longevity in Model Organisms
- Single-cell and spatial transcriptomics
- Autophagy in Disease and Therapy
- ATP Synthase and ATPases Research
- Telomeres, Telomerase, and Senescence
- CRISPR and Genetic Engineering
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Adipose Tissue and Metabolism
- Ubiquitin and proteasome pathways
- Diet and metabolism studies
- Sirtuins and Resveratrol in Medicine
- RNA Research and Splicing
- Metabolism and Genetic Disorders
- Immune cells in cancer
- Cytomegalovirus and herpesvirus research
- RNA regulation and disease
- MicroRNA in disease regulation
- GDF15 and Related Biomarkers
- Cardiac Fibrosis and Remodeling
- Virus-based gene therapy research
- Cardiomyopathy and Myosin Studies
- Genetics and Neurodevelopmental Disorders
- interferon and immune responses
Institute of Zoology
2018-2025
Chinese Academy of Sciences
2018-2025
State Key Laboratory of Membrane Biology
2024-2025
University of Chinese Academy of Sciences
2018-2025
Institute for Stem Cell Biology and Regenerative Medicine
2024
Center for Excellence in Molecular Cell Science
2018-2024
State Key Laboratory of Stem Cell and Reproductive Biology
2024
Washington University in St. Louis
2012-2022
Capital Medical University
2020
Center for Life Sciences
2020
The National Genomics Data Center (NGDC), part of the China for Bioinformation (CNCB), provides a family database resources to support global research in both academia and industry. With explosively accumulated multi-omics data at ever-faster rates, CNCB-NGDC is constantly scaling up updating its core through big archive, curation, integration analysis. In past year, efforts have been made synthesize growing knowledge, particularly single-cell omics precision medicine research, series newly...
A change of heart (mitochondria) Mitochondria provide an essential source energy to drive cellular processes and are particularly important in muscle cells (see the Perspective by Gottlieb Bernstein). After birth, availability oxygen nutrients organs tissues changes. This invokes changes metabolism. Gong et al. studied developmental transitions mouse mitochondria soon after birth. were replaced wholesale via mitophagy cardiomyocytes over first 3 weeks Preventing this turnover interfering...
Abstract Age-associated changes in immune cells have been linked to an increased risk for infection. However, a global and detailed characterization of the that human circulating undergo with age is lacking. Here, we combined scRNA-seq, mass cytometry scATAC-seq compare cell types peripheral blood collected from young old subjects patients COVID-19. We found landscape was reprogrammed characterized by T polarization naive memory effector, cytotoxic, exhausted regulatory cells, along late...
Organismal aging is driven by interconnected molecular changes encompassing internal and extracellular factors. Combinational analysis of high-throughput 'multi-omics' datasets (gathering information from genomics, epigenomics, transcriptomics, proteomics, metabolomics pharmacogenomics), at either populational or single-cell levels, can provide a multi-dimensional, integrated profile the heterogeneous process with unprecedented throughput detail. These new strategies allow for exploration...
Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened contribute to the aging process is largely unknown. In human senescent cells, we found that HERVK (HML-2), most recently integrated ERVs, are unlocked transcribe genes produce retrovirus-like particles (RVLPs). These RVLPs constitute a transmissible message elicit senescence phenotypes young which be blocked by neutralizing antibodies. The...
Rationale: The role of Parkin in hearts is unclear. Germ-line knockout mice have normal hearts, but protective cardiac ischemia. Parkin-mediated mitophagy reportedly either irrelevant, or a major factor, the lethal cardiomyopathy evoked by myocyte–specific interruption dynamin-related protein 1 (Drp1)-mediated mitochondrial fission. Objective: To understand and fission–defective adult mouse hearts. Methods Results: mRNA were present at low levels upregulated after myocyte–directed Drp1 gene...
Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase linked to a broad range of physiological and pathological processes, including aging aging-related diseases. However, the role SIRT3 in regulating human stem cell homeostasis remains unclear. Here we found that expression was downregulated senescent mesenchymal cells (hMSCs). CRISPR/Cas9-mediated depletion led compromised nuclear integrity, loss heterochromatin accelerated senescence hMSCs. Further analysis indicated interacted with envelope...
Inactivation of the histone acetyltransferase gene KAT7 prolongs survival in naturally aged mice and progeroid that age prematurely.
Regenerative capacity declines throughout evolution and with age. In this study, we asked whether metabolic programs underlying regenerative capability might be conserved across species, if so, such drivers harnessed to promote tissue repair. To end, conducted metabolomic analyses in two vertebrate organ regeneration models: the axolotl limb blastema antler stem cells. further reveal why young individuals have higher than elderly, also constructed profiles for primate juvenile aged tissues,...
In-depth profiling of genetic variations in the gut microbiome is highly desired for understanding its functionality and impacts on host health disease. Here, by harnessing long read advantage provided Oxford Nanopore Technology (ONT), we characterize fine-scale structural (SVs) hundreds microbiomes from healthy humans. ONT reads dramatically improve quality metagenomic assemblies, enable reliable detection a large, expanded set variation types (notably including large insertions...
Aberrant release of mitochondrial reactive oxygen species (mtROS) in response to cellular stress is well known for promoting cancer progression. However, precise molecular mechanism by which mtROS contribute epithelial progression remains only partially understood. Here, using colorectal (CRC) models, we show that upon sensing excessive mtROS, phosphatase PGAM5, normally localizes the mitochondria, undergoes aberrant cleavage presenilin-associated rhomboid-like protein (PARL), becoming...
Mitochondrial reactive oxygen species (ROS) are implicated in aging, chronic degenerative neurological syndromes, and myopathies. On the basis of free radical hypothesis, dietary, pharmacological, genetic ROS suppression has been tested to minimize tissue damage, with remarkable therapeutic efficacy. The effects mitochondrial-specific primary mitophagic dysfunction unknown.An vivo dose-ranging analysis an experimental cardiomyopathy provoked by defective mitochondrial clearance.Mice lacking...
Cellular senescence is a driver of various aging-associated disorders, including osteoarthritis. Here, we identified critical role for Yes-associated protein (YAP), major effector Hippo signaling, in maintaining younger state human mesenchymal stem cells (hMSCs) and ameliorating osteoarthritis mice. Clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR associated 9 nuclease (Cas9)-mediated knockout (KO) YAP hMSCs resulted premature cellular senescence. Mechanistically,...