npj Regenerative Medicine最新文献_第2页

Regeneration-specific promoter switching facilitates Mest expression in the mouse digit tip to modulate neutrophil response. 再生特异性启动子转换促进了小鼠指尖Mest的表达，从而调节中性粒细胞的反应。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-10-28 DOI: 10.1038/s41536-024-00376-w

Vivian Jou, Sophia M Peña, Jessica A Lehoczky

{"title":"Regeneration-specific promoter switching facilitates Mest expression in the mouse digit tip to modulate neutrophil response.","authors":"Vivian Jou, Sophia M Peña, Jessica A Lehoczky","doi":"10.1038/s41536-024-00376-w","DOIUrl":"10.1038/s41536-024-00376-w","url":null,"abstract":"The mouse digit tip regenerates following amputation, a process mediated by a cellularly heterogeneous blastema. We previously found the gene Mest to be highly expressed in mesenchymal cells of the blastema and a strong candidate pro-regenerative gene. We now show Mest digit expression is regeneration-specific and not upregulated in post-amputation fibrosing proximal digits. Mest homozygous knockout mice exhibit delayed bone regeneration though no phenotype is found in paternal knockout mice, inconsistent with the defined maternal genomic imprinting of Mest. We demonstrate that promoter switching, not loss of imprinting, regulates biallelic Mest expression in the blastema and does not occur during embryogenesis, indicating a regeneration-specific mechanism. Requirement for Mest expression is tied to modulating neutrophil response, as revealed by scRNAseq and FACS comparing wildtype and knockout blastemas. Collectively, the imprinted gene Mest is required for proper digit tip regeneration and its blastema expression is facilitated by promoter switching for biallelic expression.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"32"},"PeriodicalIF":6.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11519450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration. 他汀类药物与基质结合纳米颗粒的免疫调节作用可促进视神经再生。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-10-26 DOI: 10.1038/s41536-024-00374-y

Gregory P Campbell, Dwarkesh Amin, Kristin Hsieh, George S Hussey, Anthony J St Leger, Jeffrey M Gross, Stephen F Badylak, Takaaki Kuwajima

{"title":"Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration.","authors":"Gregory P Campbell, Dwarkesh Amin, Kristin Hsieh, George S Hussey, Anthony J St Leger, Jeffrey M Gross, Stephen F Badylak, Takaaki Kuwajima","doi":"10.1038/s41536-024-00374-y","DOIUrl":"10.1038/s41536-024-00374-y","url":null,"abstract":"Modulating inflammation is critical to enhance nerve regeneration after injury. However, clinically applicable regenerative therapies that modulate inflammation have not yet been established. Here, we demonstrate synergistic effects of the combination of an HMG-CoA reductase inhibitor, statin/fluvastatin and critical components of the extracellular matrix, Matrix-Bound Nanovesicles (MBV) to enhance axon regeneration and neuroprotection after mouse optic nerve injury. Mechanistically, co-intravitreal injections of fluvastatin and MBV robustly promote infiltration of monocytes and neutrophils, which lead to RGC protection and axon regeneration. Furthermore, monocyte infiltration is triggered by elevated expression of CCL2, a chemokine, in the superficial layer of the retina after treatment with a combination of fluvastatin and MBV or IL-33, a cytokine contained within MBV. Finally, this therapy can be further combined with AAV-based gene therapy blocking anti-regenerative pathways in RGCs to extend regenerated axons. These data highlight novel molecular insights into the development of immunomodulatory regenerative therapy.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"31"},"PeriodicalIF":6.4,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11513974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A latent Axin2⁺/Scx⁺ progenitor pool is the central organizer of tendon healing. 潜伏的 Axin2+/Scx+ 祖细胞池是肌腱愈合的核心组织者。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-10-17 DOI: 10.1038/s41536-024-00370-2

Mor Grinstein, Stephanie L Tsai, Daniel Montoro, Benjamin R Freedman, Heather L Dingwall, Steffany Villaseñor, Ken Zou, Moshe Sade-Feldman, Miho J Tanaka, David J Mooney, Terence D Capellini, Jayaraj Rajagopal, Jenna L Galloway

{"title":"A latent Axin2+/Scx+ progenitor pool is the central organizer of tendon healing.","authors":"Mor Grinstein, Stephanie L Tsai, Daniel Montoro, Benjamin R Freedman, Heather L Dingwall, Steffany Villaseñor, Ken Zou, Moshe Sade-Feldman, Miho J Tanaka, David J Mooney, Terence D Capellini, Jayaraj Rajagopal, Jenna L Galloway","doi":"10.1038/s41536-024-00370-2","DOIUrl":"https://doi.org/10.1038/s41536-024-00370-2","url":null,"abstract":"A tendon's ordered extracellular matrix (ECM) is essential for transmitting force but is also highly prone to injury. How tendon cells embedded within and surrounding this dense ECM orchestrate healing is not well understood. Here, we identify a specialized quiescent Scx+/Axin2+ population in mouse and human tendons that initiates healing and is a major functional contributor to repair. Axin2+ cells express stem cell markers, expand in vitro, and have multilineage differentiation potential. Following tendon injury, Axin2+-descendants infiltrate the injury site, proliferate, and differentiate into tenocytes. Transplantation assays of Axin2-labeled cells into injured tendons reveal their dual capacity to significantly proliferate and differentiate yet retain their Axin2+ identity. Specific loss of Wnt secretion in Axin2+ or Scx+ cells disrupts their ability to respond to injury, severely compromising healing. Our work highlights an unusual paradigm, wherein specialized Axin2+/Scx+ cells rely on self-regulation to maintain their identity as key organizers of tissue healing.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"30"},"PeriodicalIF":6.4,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11487078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142480633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A computational model reveals an early transient decrease in fiber cross-linking that unlocks adult regeneration. 一个计算模型揭示了纤维交联的早期瞬时减少，从而开启了成体再生。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-10-15 DOI: 10.1038/s41536-024-00373-z

Anastasia Pacary, Diane Peurichard, Laurence Vaysse, Paul Monsarrat, Clémence Bolut, Adeline Girel, Christophe Guissard, Anne Lorsignol, Valérie Planat-Benard, Jenny Paupert, Marielle Ousset, Louis Casteilla

{"title":"A computational model reveals an early transient decrease in fiber cross-linking that unlocks adult regeneration.","authors":"Anastasia Pacary, Diane Peurichard, Laurence Vaysse, Paul Monsarrat, Clémence Bolut, Adeline Girel, Christophe Guissard, Anne Lorsignol, Valérie Planat-Benard, Jenny Paupert, Marielle Ousset, Louis Casteilla","doi":"10.1038/s41536-024-00373-z","DOIUrl":"https://doi.org/10.1038/s41536-024-00373-z","url":null,"abstract":"The decline in regeneration efficiency after birth in mammals is a significant roadblock for regenerative medicine in tissue repair. We previously developed a computational agent based-model (ABM) that recapitulates mechanical interactions between cells and the extracellular-matrix (ECM), to investigate key drivers of tissue repair in adults. Time calibration alongside a parameter sensitivity analysis of the model suggested that an early and transient decrease in ECM cross-linking guides tissue repair toward regeneration. Consistent with the computational model, transient inhibition or stimulation of fiber cross-linking for the first six days after subcutaneous adipose tissue (AT) resection in adult mice led to regenerative or scar healing, respectively. Therefore, this work positions the computational model as a predictive tool for tissue regeneration that with further development will behave as a digital twin of our in vivo model. In addition, it opens new therapeutic approaches targeting ECM cross-linking to induce tissue regeneration in adult mammals.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"29"},"PeriodicalIF":6.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142480632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Infected wound repair correlates with collagen I induction and NOX2 activation by cold atmospheric plasma. 感染伤口的修复与冷大气等离子体诱导胶原蛋白 I 和激活 NOX2 有关。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-10-02 DOI: 10.1038/s41536-024-00372-0

Océane Blaise, Constance Duchesne, Elena Capuzzo, Marie-Anne Nahori, Julien Fernandes, Michael G Connor, Mélanie A Hamon, Javier Pizarro-Cerda, Jean-Jacques Lataillade, Colin McGuckin, Antoine Rousseau, Sébastien Banzet, Olivier Dussurget, Nadira Frescaline

{"title":"Infected wound repair correlates with collagen I induction and NOX2 activation by cold atmospheric plasma.","authors":"Océane Blaise, Constance Duchesne, Elena Capuzzo, Marie-Anne Nahori, Julien Fernandes, Michael G Connor, Mélanie A Hamon, Javier Pizarro-Cerda, Jean-Jacques Lataillade, Colin McGuckin, Antoine Rousseau, Sébastien Banzet, Olivier Dussurget, Nadira Frescaline","doi":"10.1038/s41536-024-00372-0","DOIUrl":"10.1038/s41536-024-00372-0","url":null,"abstract":"Cold atmospheric plasma (CAP) is a promising complement to tissue repair and regenerative medicine approaches. CAP has therapeutic potential in infected cutaneous wounds by mechanisms which remain enigmatic. Here, CAP is shown to activate phagocyte NADPH oxidase complex NOX2. CAP induced increased intracellular reactive oxygen species, alleviated by NOX2 inhibitors. Genetic and pharmacological inhibitions of NOX2 in macrophages and bioengineered skin infected with Staphylococcus aureus and treated with CAP reduced intracellular oxidants and increased bacterial survival. CAP triggered Rac activation and phosphorylation of p40phox and p47phox required for NOX2 assembly and activity. Furthermore, CAP induced collagen I expression by fibroblasts. Infection and healing kinetics showed that murine skin wounds infected with S. aureus and treated with CAP are characterized by decreased bacterial burden, increased length of neoepidermis and extracellular matrix formation. Collectively, our findings identify mechanisms triggered by CAP that subdue infection and result in enhanced repair following skin injury.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"28"},"PeriodicalIF":6.4,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Utilising an in silico model to predict outcomes in senescence-driven acute liver injury. 利用硅学模型预测衰老驱动的急性肝损伤的结果。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-09-30 DOI: 10.1038/s41536-024-00371-1

Candice Ashmore-Harris, Evangelia Antonopoulou, Rhona E Aird, Tak Yung Man, Simon M Finney, Annelijn M Speel, Wei-Yu Lu, Stuart J Forbes, Victoria L Gadd, Sarah L Waters

{"title":"Utilising an in silico model to predict outcomes in senescence-driven acute liver injury.","authors":"Candice Ashmore-Harris, Evangelia Antonopoulou, Rhona E Aird, Tak Yung Man, Simon M Finney, Annelijn M Speel, Wei-Yu Lu, Stuart J Forbes, Victoria L Gadd, Sarah L Waters","doi":"10.1038/s41536-024-00371-1","DOIUrl":"10.1038/s41536-024-00371-1","url":null,"abstract":"Currently liver transplantation is the only treatment option for liver disease, but organ availability cannot meet patient demand. Alternative regenerative therapies, including cell transplantation, aim to modulate the injured microenvironment from inflammation and scarring towards regeneration. The complexity of the liver injury response makes it challenging to identify suitable therapeutic targets when relying on experimental approaches alone. Therefore, we adopted a combined in vivo-in silico approach and developed an ordinary differential equation model of acute liver disease able to predict the host response to injury and potential interventions. The Mdm2fl/fl mouse model of senescence-driven liver injury was used to generate a quantitative dynamic characterisation of the key cellular players (macrophages, endothelial cells, myofibroblasts) and extra cellular matrix involved in liver injury. This was qualitatively captured by the mathematical model. The mathematical model was then used to predict injury outcomes in response to milder and more severe levels of senescence-induced liver injury and validated with experimental in vivo data. In silico experiments using the validated model were then performed to interrogate potential approaches to enhance regeneration. These predicted that increasing the rate of macrophage phenotypic switch or increasing the number of pro-regenerative macrophages in the system will accelerate the rate of senescent cell clearance and resolution. These results showcase the potential benefits of mechanistic mathematical modelling for capturing the dynamics of complex biological systems and identifying therapeutic interventions that may enhance our understanding of injury-repair mechanisms and reduce translational bottlenecks.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"26"},"PeriodicalIF":6.4,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142332262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-inflammatory Prowess of endothelial progenitor cells in the realm of biology and medicine. 内皮祖细胞在生物学和医学领域的抗炎能力。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-09-30 DOI: 10.1038/s41536-024-00365-z

Mehdi Hassanpour, Amankeldi A Salybkov, Shuzo Kobayashi, Takayuki Asahara

{"title":"Anti-inflammatory Prowess of endothelial progenitor cells in the realm of biology and medicine.","authors":"Mehdi Hassanpour, Amankeldi A Salybkov, Shuzo Kobayashi, Takayuki Asahara","doi":"10.1038/s41536-024-00365-z","DOIUrl":"10.1038/s41536-024-00365-z","url":null,"abstract":"Endothelial inflammation plays a crucial role in vascular-related diseases, a leading cause of global mortality. Among various cellular players, endothelial progenitor cells (EPCs) emerge as non-differentiated endothelial cells circulating in the bloodstream. Recent evidence highlights the transformative role of EPCs in shifting from an inflammatory/immunosuppressive crisis to an anti-inflammatory/immunomodulatory response. Despite the importance of these functions, the regulatory mechanisms governing EPC activities and their physiological significance in vascular regenerative medicine remain elusive. Surprisingly, the current literature lacks a comprehensive review of EPCs' effects on inflammatory processes. This narrative review aims to fill this gap by exploring the cutting-edge role of EPCs against inflammation, from molecular intricacies to broader medical perspectives. By examining how EPCs modulate inflammatory responses, we aim to unravel their anti-inflammatory significance in vascular regenerative medicine, deepening insights into EPCs' molecular mechanisms and guiding future therapeutic strategies targeting vascular-related diseases.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"27"},"PeriodicalIF":6.4,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142332260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integrative cartilage repair using acellular allografts for engineered structure and surface lubrication in vivo. 利用细胞异体移植物进行体内软骨结构和表面润滑的综合修复。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-09-28 DOI: 10.1038/s41536-024-00367-x

Jeanne E Barthold, Luyao Cai, Kaitlin P McCreery, Kristine M Fischenich, Kevin N Eckstein, Virginia L Ferguson, Nancy C Emery, Gert Breur, Corey P Neu

{"title":"Integrative cartilage repair using acellular allografts for engineered structure and surface lubrication in vivo.","authors":"Jeanne E Barthold, Luyao Cai, Kaitlin P McCreery, Kristine M Fischenich, Kevin N Eckstein, Virginia L Ferguson, Nancy C Emery, Gert Breur, Corey P Neu","doi":"10.1038/s41536-024-00367-x","DOIUrl":"https://doi.org/10.1038/s41536-024-00367-x","url":null,"abstract":"The repair of articular cartilage after damage is challenging, and decellularized tissue offers a possible treatment option to promote regeneration. Here, we show that acellular osteochondral allografts improve integrative cartilage repair compared to untreated defects after 6 months in an ovine model. Functional measures of intratissue strain/structure assessed by MRI demonstrate similar biomechanics of implants and native cartilage. Compared to native tissue and defects, the structure, composition, and tribology of acellular allografts preserve surface roughness and lubrication, material properties under compression and relaxation, compositional ratios of collagen:glycosaminoglycan and collagen:phosphate, and relative composition of types I/II collagen. While high cellularity was observed in bone regions and integration zones between cartilage-allografts, recellularization of chondral implants was inconsistent, with cell migration typically less than ~750 µm into the dense decellularized tissue, possibly limiting long-term cellular maintenance. Our results demonstrate the structural and biomechanical efficacy of acellular allografts for at least six months in vivo.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"9 1","pages":"25"},"PeriodicalIF":6.4,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142332261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Implication of CXCR2-Src axis in the angiogenic and osteogenic effects of FP-TEB. CXCR2-Src轴在FP-TEB的血管生成和成骨效应中的作用。

IF 6.4 1区医学

npj Regenerative Medicine Pub Date : 2024-09-20 DOI: 10.1038/s41536-024-00364-0

Sihao He, Tianyong Hou, Jiangling Zhou, Bo Yu, Juan Cai, Fei Luo, Jianzhong Xu, Junchao Xing

引用次数: 0

Calorie restriction and rapamycin distinctly restore non-canonical ORF translation in the muscles of aging mice 卡路里限制和雷帕霉素可明显恢复衰老小鼠肌肉中的非规范 ORF 翻译

IF 7.2 1区医学

npj Regenerative Medicine Pub Date : 2024-09-19 DOI: 10.1038/s41536-024-00369-9

Nitish Mittal, Meric Ataman, Lionel Tintignac, Daniel J. Ham, Lena Jörin, Alexander Schmidt, Michael Sinnreich, Markus A. Ruegg, Mihaela Zavolan

{"title":"Calorie restriction and rapamycin distinctly restore non-canonical ORF translation in the muscles of aging mice","authors":"Nitish Mittal, Meric Ataman, Lionel Tintignac, Daniel J. Ham, Lena Jörin, Alexander Schmidt, Michael Sinnreich, Markus A. Ruegg, Mihaela Zavolan","doi":"10.1038/s41536-024-00369-9","DOIUrl":"https://doi.org/10.1038/s41536-024-00369-9","url":null,"abstract":"Loss of protein homeostasis is one of the hallmarks of aging. As such, interventions that restore proteostasis should slow down the aging process and improve healthspan. Two of the most broadly used anti-aging interventions that are effective in organisms from yeast to mammals are calorie restriction (CR) and rapamycin (RM) treatment. To identify the regulatory mechanisms by which these interventions improve the protein homeostasis, we carried out ribosome footprinting in the muscle of mice aged under standard conditions, or under long-term treatment with CR or RM. We found that the treatments distinctly impact the non-canonical translation, RM primarily remodeling the translation of upstream open reading frames (uORFs), while CR restores stop codon readthrough and the translation of downstream ORFs. Proteomics analysis revealed the expression of numerous non-canonical ORFs at the protein level. The corresponding peptides may provide entry points for therapies aiming to maintain muscle function and extend health span.","PeriodicalId":54236,"journal":{"name":"npj Regenerative Medicine","volume":"4 1","pages":""},"PeriodicalIF":7.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142263061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0