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2.
Stem Cell Res Ther ; 13(1): 71, 2022 02 15.
Article in English | MEDLINE | ID: covidwho-1759775

ABSTRACT

Pulmonary fibrosis is a devastating disease that eventually leads to death and respiratory failure. Despite the wide range of drugs, including corticosteroids, endothelin antagonist, and pirfenidone, there is no effective treatment, and the only main goal of treatment is to alleviate the symptoms as much as possible to slow down the progression of the disease and improve the quality of life. Lung transplantation may be a treatment option for a few people if pulmonary fibrosis develops and there is no established treatment. Pulmonary fibrosis caused by the COVID19 virus is another problem that we face in most patients despite the efforts of the international medical communities. Therefore, achieving alternative treatment for patients is a great success. Today, basic research using stem cells on pulmonary fibrosis has published promising results. New stem cell-based therapies can be helpful in patients with pulmonary fibrosis. Wharton jelly-derived mesenchymal stem cells are easily isolated in large quantities and made available for clinical trials without causing ethical problems. These cells have higher flexibility and proliferation potential than other cells isolated from different sources and differentiated into various cells in laboratory environments. More clinical trials are needed to determine the safety and efficacy of these cells. This study will investigate the cellular and molecular mechanisms and possible effects of Wharton jelly-derived mesenchymal stem cells in pulmonary fibrosis.


Subject(s)
COVID-19 , Mesenchymal Stem Cells , Pulmonary Fibrosis , Wharton Jelly , Cell Differentiation , Humans , Pulmonary Fibrosis/therapy , Quality of Life
3.
J Zhejiang Univ Sci B ; 23(2): 102-122, 2022 Feb 15.
Article in English | MEDLINE | ID: covidwho-1706587

ABSTRACT

Molecular hydrogen exerts biological effects on nearly all organs. It has anti-oxidative, anti-inflammatory, and anti-aging effects and contributes to the regulation of autophagy and cell death. As the primary organ for gas exchange, the lungs are constantly exposed to various harmful environmental irritants. Short- or long-term exposure to these harmful substances often results in lung injury, causing respiratory and lung diseases. Acute and chronic respiratory diseases have high rates of morbidity and mortality and have become a major public health concern worldwide. For example, coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global pandemic. An increasing number of studies have revealed that hydrogen may protect the lungs from diverse diseases, including acute lung injury, chronic obstructive pulmonary disease, asthma, lung cancer, pulmonary arterial hypertension, and pulmonary fibrosis. In this review, we highlight the multiple functions of hydrogen and the mechanisms underlying its protective effects in various lung diseases, with a focus on its roles in disease pathogenesis and clinical significance.


Subject(s)
COVID-19/immunology , COVID-19/therapy , Hydrogen/therapeutic use , Lung Diseases/therapy , Acute Lung Injury , Aging , Animals , Anti-Inflammatory Agents , Antioxidants/chemistry , Asthma/therapy , Autophagy , COVID-19/drug therapy , Humans , Hypertension, Pulmonary/therapy , Inflammation , Lung Neoplasms/therapy , Mice , Oxidative Stress , Pulmonary Disease, Chronic Obstructive/therapy , Pulmonary Fibrosis/therapy , Pyroptosis , Reactive Oxygen Species
4.
Medicine (Baltimore) ; 101(3): e28639, 2022 Jan 21.
Article in English | MEDLINE | ID: covidwho-1642427

ABSTRACT

ABSTRACT: The development of pulmonary fibrosis is a rare complication of the novel coronavirus disease 2019 (COVID-19). Limited information is available in the literature about that, and the present study aimed to address this gap.This case-control study included 64 patients with post-COVID-19 pulmonary fibrosis who were hospitalized for COVID-19.The percentage of patients aged ≥65 years (44%) who demised was higher than those who survived (25%). Male patients (62%) had higher mortality than female patients (37%). The most frequently reported clinical symptoms were shortness of breath (98%), cough (91%), and fever (70%). Most COVID-19 patients with pulmonary fibrosis (81%) were admitted to an intensive care unit (ICU), and 63% required mechanical ventilation. Bilateral lung infiltrates (94%), "ground glass" opacity (91%), "honeycomb" lung (25%), and pulmonary consolidation (9%) were commonly identified in COVID-19 patients with pulmonary fibrosis who survived. The findings for computed tomography and dyspnea scale were significantly higher in severe cases admitted to the ICU who required mechanical ventilation. A higher computerized tomography score also correlated significantly with a longer duration of stay in hospital and a higher degree of dyspnea. Half of the COVID-19 patients with pulmonary fibrosis (50%) who survived required oxygen therapy, and those with "honeycomb" lung required long-term oxygen therapy to a far greater extent than others. Cox regression revealed that smoking and asthma were significantly associated with ICU admission and the risk of mortality.Post-COVID-19 pulmonary fibrosis is a severe complication that leads to permanent lung damage or death.


Subject(s)
COVID-19/complications , Lung/diagnostic imaging , Adrenal Cortex Hormones/therapeutic use , Anticoagulants/therapeutic use , COVID-19/epidemiology , Case-Control Studies , Cough/etiology , Dyspnea/etiology , Female , Fever/etiology , Humans , Intensive Care Units , Male , Oxygen , Prednisolone/therapeutic use , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , Retrospective Studies , SARS-CoV-2 , Saudi Arabia/epidemiology , Tomography, X-Ray Computed , Vitamins/therapeutic use
5.
Dtsch Med Wochenschr ; 146(13-14): 927-932, 2021 Jul.
Article in German | MEDLINE | ID: covidwho-1493274

ABSTRACT

Acute COVID-19 pneumonia may result in persistent changes with various imaging and histopathological patterns, including organizing pneumonia and pulmonary fibrosis. In addition, SARS-CoV-2 infection is associated with increased risk of pulmonary vascular endothelialitis and thrombosis. Herein, current findings on pulmonary consequences of COVID-19 with implications for clinical management are summarized based on a selective literature review.


Subject(s)
COVID-19/complications , Cryptogenic Organizing Pneumonia/complications , Pneumonia, Viral/complications , Pulmonary Fibrosis/complications , Acute Disease , COVID-19/diagnostic imaging , COVID-19/therapy , Cryptogenic Organizing Pneumonia/diagnostic imaging , Cryptogenic Organizing Pneumonia/therapy , Follow-Up Studies , Humans , Pneumonia, Viral/diagnostic imaging , Pneumonia, Viral/therapy , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/therapy
6.
Int J Biol Sci ; 17(6): 1565-1573, 2021.
Article in English | MEDLINE | ID: covidwho-1206427

ABSTRACT

Dysregulated immune response and abnormal repairment could cause secondary pulmonary fibrosis of varying severity in COVID-19, especially for the elders. The Krebs Von den Lungen-6 (KL-6) as a sensitive marker reflects the degree of fibrosis and this study will focus on analyzing the evaluative efficacy and predictive role of KL-6 in COVID-19 secondary pulmonary fibrosis. The study lasted more than three months and included total 289 COVID-19 patients who were divided into moderate (n=226) and severe groups (n=63) according to the severity of illness. Clinical information such as inflammation indicators, radiological results and lung function tests were collected. The time points of nucleic acid test were also recorded. Furthermore, based on Chest radiology detection, it was identified that 80 (27.7%) patients developed reversible pulmonary fibrosis and 34 (11.8%) patients developed irreversible pulmonary fibrosis. Receiver operating characteristic (ROC) curve analysis shows that KL-6 could diagnose the severity of COVID-19 (AUC=0.862) and predict the occurrence of pulmonary fibrosis (AUC = 0.741) and irreversible pulmonary fibrosis (AUC=0.872). Importantly, the cross-correlation analysis demonstrates that KL-6 rises earlier than the development of lung radiology fibrosis, thus also illuminating the predictive function of KL-6. We set specific values (505U/mL and 674U/mL) for KL-6 in order to assess the risk of pulmonary fibrosis after SARS-CoV-2 infection. The survival curves for days in hospital show that the higher the KL-6 levels, the longer the hospital stay (P<0.0001). In conclusion, KL-6 could be used as an important predictor to evaluate the secondary pulmonary fibrosis degree for COVID-19.


Subject(s)
COVID-19/complications , Mucin-1/metabolism , Pulmonary Fibrosis/complications , Adult , Aged , COVID-19/virology , Female , Humans , Male , Middle Aged , Pulmonary Fibrosis/therapy , Risk Factors , SARS-CoV-2/isolation & purification
7.
Expert Rev Respir Med ; 15(6): 791-803, 2021 06.
Article in English | MEDLINE | ID: covidwho-1203511

ABSTRACT

Introduction: Coronavirus disease 2019 (COVID-19) is still increasing worldwide, and as a result, the number of patients with pulmonary fibrosis secondary to COVID-19 will expand over time. Risk factors, histopathological characterization, pathophysiology, prevalence, and management of post-COVID-19 pulmonary fibrosis are poorly understood, and few studies have addressed these issues.Areas covered:This article reviews the current evidence regarding post-COVID-19 pulmonary fibrosis, with an emphasis on the potential risk factors, histopathology, pathophysiology, functional and tomographic features, and potential therapeutic modalities. A search on the issue was performed in the MEDLINE, Embase, and SciELO databases and the Cochrane library between 1 December 2019, and 25 January 2021. Studies were reviewed and relevant topics were incorporated into this narrative review. Expert opinion: Pulmonary sequelae may occur secondary to COVID-19, which needs to be included as a potential etiology in the current differential diagnosis of pulmonary fibrosis. Therefore, serial clinical, tomographic, and functional screening for pulmonary fibrosis is recommended after COVID-19, mainly in patients with pulmonary involvement in the acute phase of the disease. Further studies are necessary to determine the risk factors, markers, pathophysiology, and appropriate management of post-COVID-19 pulmonary fibrosis.


Subject(s)
COVID-19/complications , Pulmonary Fibrosis/etiology , COVID-19/diagnosis , COVID-19/pathology , COVID-19/therapy , Databases, Factual , Diagnosis, Differential , Disease Progression , Humans , Lung/pathology , Lung/virology , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , Risk Factors , SARS-CoV-2/physiology , Severity of Illness Index , Tomography, X-Ray Computed/methods
8.
Stem Cell Res Ther ; 12(1): 230, 2021 04 12.
Article in English | MEDLINE | ID: covidwho-1192728

ABSTRACT

BACKGROUND: Pulmonary fibrosis (PF), the end point of interstitial lung diseases, is characterized by myofibroblast over differentiation and excessive extracellular matrix accumulation, leading to progressive organ dysfunction and usually a terminal outcome. Studies have shown that umbilical cord-derived mesenchymal stromal cells (uMSCs) could alleviate PF; however, the underlying mechanism remains to be elucidated. METHODS: The therapeutic effects of uMSC-derived extracellular vesicles (uMSC-EVs) on PF were evaluated using bleomycin (BLM)-induced mouse models. Then, the role and mechanism of uMSC-EVs in inhibiting myofibroblast differentiation were investigated in vivo and in vitro. RESULTS: Treatment with uMSC-EVs alleviated the PF and enhanced the proliferation of alveolar epithelial cells in BLM-induced mice, thus improved the life quality, including the survival rate, body weight, fibrosis degree, and myofibroblast over differentiation of lung tissue. Moreover, these effects of uMSC-EVs on PF are likely achieved by inhibiting the transforming growth factor-ß (TGF-ß) signaling pathway, evidenced by decreased expression levels of TGF-ß2 and TGF-ßR2. Using mimics of uMSC-EV-specific miRNAs, we found that miR-21 and miR-23, which are highly enriched in uMSC-EVs, played a critical role in inhibiting TGF-ß2 and TGF-ßR2, respectively. CONCLUSION: The effects of uMSCs on PF alleviation are likely achieved via EVs, which reveals a new role of uMSC-EV-derived miRNAs, opening a novel strategy for PF treatment in the clinical setting.


Subject(s)
Extracellular Vesicles , Mesenchymal Stem Cells , Pulmonary Fibrosis , Animals , Bleomycin/toxicity , Mice , Pulmonary Fibrosis/chemically induced , Pulmonary Fibrosis/genetics , Pulmonary Fibrosis/therapy , Signal Transduction , Transforming Growth Factor beta/genetics , Transforming Growth Factors , Umbilical Cord
9.
Cell Transplant ; 30: 963689721996217, 2021.
Article in English | MEDLINE | ID: covidwho-1181030

ABSTRACT

COVID-19 has spread worldwide, including the United States, United Kingdom, and Italy, along with its site of origin in China, since 2020. The virus was first found in the Wuhan seafood market at the end of 2019, with a controversial source. The clinical symptoms of COVID-19 include fever, cough, and respiratory tract inflammation, with some severe patients developing an acute and chronic lung injury, such as acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF). It has already claimed approximately 300 thousand human lives and the number is still on the rise; the only way to prevent the infection is to be safe till vaccines and reliable treatments develop. In previous studies, the use of mesenchymal stem cells (MSCs) in clinical trials had been proven to be effective in immune modulation and tissue repair promotion; however, their efficacy in treating COVID-19 remains underestimated. Here, we report the findings from past experiences of SARS and MSCs, and how SARS could also induce PF. Such studies may help to understand the rationale for the recent cell-based therapies for COVID-19.


Subject(s)
COVID-19/complications , Mesenchymal Stem Cell Transplantation , Pulmonary Fibrosis/etiology , Animals , COVID-19/blood , COVID-19/pathology , COVID-19/therapy , Coronavirus/isolation & purification , Humans , Mesenchymal Stem Cell Transplantation/methods , Pulmonary Fibrosis/blood , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , Renin-Angiotensin System , SARS-CoV-2/isolation & purification , Severe Acute Respiratory Syndrome/blood , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/pathology , Severe Acute Respiratory Syndrome/therapy , Transforming Growth Factor beta/blood
10.
Eur Rev Med Pharmacol Sci ; 25(6): 2748-2751, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1173126

ABSTRACT

COVID-19 is an acute respiratory infectious disease caused by SARS-COV 2 (Severe Acute Respiratory Syndrome Coronavirus) that has become a global pandemic. COVID-19 mainly causes the respiratory complications of Acute Respiratory Distress Syndrome (ARDS), cytokine storm, and severe immune disruptions. The assays depict that though people recuperate from COVID-19, there are still symptoms that persists in the body causing discomfort, which is the consequence of the viral infection due to severe immune disruptions. Upon various difficulties of post COVID-19, the pulmonary fibrosis is the stumbling block in the lungs causing severe damage. In this review, we have shown the effectiveness and importance of the Hepatocyte Growth Factor (HGF) secreted by Mesenchymal Stem Cell (MSC) therapy on selective stoppage of the Transforming Growth Factor-Beta (TGF-ß) signalling pathway by causing immunomodulatory effects that ameliorate the pulmonary fibrosis through paracrine signalling. However, more pilot studies have to be carried out to determine the efficacy and outcomes of the re-emerging complication.


Subject(s)
COVID-19/epidemiology , Mesenchymal Stem Cell Transplantation/methods , Mesenchymal Stem Cells/cytology , Pulmonary Fibrosis/therapy , Pulmonary Fibrosis/virology , COVID-19/transmission , COVID-19/virology , Global Health , Humans , Pulmonary Fibrosis/epidemiology , SARS-CoV-2/isolation & purification
11.
Infect Dis Poverty ; 10(1): 31, 2021 Mar 18.
Article in English | MEDLINE | ID: covidwho-1140517

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to a significant number of mortalities worldwide. COVID-19 poses a serious threat to human life. The clinical manifestations of COVID-19 are diverse and severe and 20% of infected patients are reported to be in a critical condition. A loss in lung function and pulmonary fibrosis are the main manifestations of patients with the severe form of the disease. The lung function is affected, even after recovery, thereby greatly affecting the psychology and well-being of patients, and significantly reducing their quality of life. METHODS: Participants must meet the following simultaneous inclusion criteria: over 18 years of age, should have recovered from severe or critical COVID-19 cases, should exhibit pulmonary fibrosis after recovery, and should exhibit Qi-Yin deficiency syndrome as indicated in the system of traditional Chinese medicine (TCM). The eligible candidates will be randomized into treatment or control groups. The treatment group will receive modern medicine (pirfenidone) plus TCM whereas the control group will be administered modern medicine plus TCM placebo. The lung function index will be continuously surveyed and recorded. By comparing the treatment effect between the two groups, the study intend to explore whether TCM can improve the effectiveness of modern medicine in patients with pulmonary fibrosis arising as a sequelae after SARS-CoV-2 infection. DISCUSSION: Pulmonary fibrosis is one of fatal sequelae for some severe or critical COVID-19 cases, some studies reveal that pirfenidone lead to a delay in the decline of forced expiratory vital capacity, thereby reducing the mortality partly. Additionally, although TCM has been proven to be efficacious in treating pulmonary fibrosis, its role in treating pulmonary fibrosis related COVID-19 has not been explored. Hence, a multicenter, parallel-group, randomized controlled, interventional, prospective clinical trial has been designed and will be conducted to determine if a new comprehensive treatment for pulmonary fibrosis related to COVID-19 is feasible and if it can improve the quality of life of patients. TRIAL REGISTRATION: This multicenter, parallel-group, randomized controlled, interventional, prospective trial was registered at the Chinese Clinical Trial Registry (ChiCTR2000033284) on 26th May 2020 (prospective registered).


Subject(s)
COVID-19/complications , COVID-19/virology , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , SARS-CoV-2 , Antiviral Agents/therapeutic use , Combined Modality Therapy , Data Analysis , Medicine, Chinese Traditional , Pulmonary Fibrosis/diagnosis , Quality of Life , Treatment Outcome
12.
Stem Cells ; 39(6): 707-722, 2021 06.
Article in English | MEDLINE | ID: covidwho-1121521

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has grown to be a global public health crisis with no safe and effective treatments available yet. Recent findings suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus pathogen that causes COVID-19, could elicit a cytokine storm that drives edema, dysfunction of the airway exchange, and acute respiratory distress syndrome in the lung, followed by acute cardiac injury and thromboembolic events leading to multiorgan failure and death. Mesenchymal stem cells (MSCs), owing to their powerful immunomodulatory abilities, have the potential to attenuate the cytokine storm and have therefore been proposed as a potential therapeutic approach for which several clinical trials are underway. Given that intravenous infusion of MSCs results in a significant trapping in the lung, MSC therapy could directly mitigate inflammation, protect alveolar epithelial cells, and reverse lung dysfunction by normalizing the pulmonary microenvironment and preventing pulmonary fibrosis. In this review, we present an overview and perspectives of the SARS-CoV-2 induced inflammatory dysfunction and the potential of MSC immunomodulation for the prevention and treatment of COVID-19 related pulmonary disease.


Subject(s)
COVID-19/immunology , Cytokine Release Syndrome/immunology , Mesenchymal Stem Cells/immunology , SARS-CoV-2/immunology , COVID-19/therapy , COVID-19/virology , Cytokine Release Syndrome/therapy , Cytokine Release Syndrome/virology , Humans , Immunomodulation , Lung/immunology , Lung/pathology , Lung/virology , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/virology , Pandemics , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/therapy , Pulmonary Fibrosis/virology , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/therapy , Respiratory Distress Syndrome/virology , SARS-CoV-2/genetics
13.
J Gene Med ; 23(3): e3318, 2021 03.
Article in English | MEDLINE | ID: covidwho-1084739

ABSTRACT

Pulmonary fibrosis is characterized by progressive and irreversible scarring in the lungs with poor prognosis and treatment. It is caused by various factors, including environmental and occupational exposures, and some rheumatic immune diseases. Even the rapid global spread of the COVID-19 pandemic can also cause pulmonary fibrosis with a high probability. Functions attributed to long non-coding RNAs (lncRNAs) make them highly attractive diagnostic and therapeutic targets in fibroproliferative diseases. Therefore, an understanding of the specific mechanisms by which lncRNAs regulate pulmonary fibrotic pathogenesis is urgently needed to identify new possibilities for therapy. In this review, we focus on the molecular mechanisms and implications of lncRNAs targeted protein-coding and non-coding genes during pulmonary fibrogenesis, and systematically analyze the communication of lncRNAs with various types of RNAs, including microRNA, circular RNA and mRNA. Finally, we propose the potential approach of lncRNA-based diagnosis and therapy for pulmonary fibrosis. We hope that understanding these interactions between protein-coding and non-coding genes will contribute to the development of lncRNA-based clinical applications for pulmonary fibrosis.


Subject(s)
Genetic Markers/genetics , Pulmonary Fibrosis/genetics , RNA, Long Noncoding/genetics , Gene Expression Regulation , Genetic Therapy/methods , Humans , MicroRNAs/genetics , Proteins/genetics , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , RNA, Circular/genetics
15.
Indian J Tuberc ; 68(3): 330-333, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-988078

ABSTRACT

After the COVID-19 outbreak, increasing number of patients worldwide who have survived COVID-19 continue to battle the symptoms of the illness, long after they have been clinically tested negative for the disease. As we battle through this pandemic, the challenging part is to manage COVID-19 sequelae which may vary from fatigue and body aches to lung fibrosis. This review addresses underlying mechanism, risk factors, course of disease and treatment option for post covid pulmonary fibrosis. Elderly patient who require ICU care and mechanical ventilation are at the highest risk to develop lung fibrosis. Currently, no fully proven options are available for the treatment of post inflammatory COVID 19 pulmonary fibrosis.


Subject(s)
COVID-19/complications , Patient Care Management , Pulmonary Fibrosis , COVID-19/epidemiology , COVID-19/therapy , Humans , Pulmonary Fibrosis/epidemiology , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , Risk Factors , SARS-CoV-2
18.
Dtsch Med Wochenschr ; 145(15): 1086-1092, 2020 Jul.
Article in German | MEDLINE | ID: covidwho-706008

ABSTRACT

The long-term sequelae of COVID-19 on are not yet predictable. Radiological and histopathological data on COVID-19 and observational studies after the SARS-CoV-1 pandemic 2003/2004 suggest that in a proportion of COVID-19 patients, functional limitations due to pulmonary fibrosis and other patterns of lung damage may persist. Systematic follow-up, based on prudent pulmonary function testing, is warranted for the correct diagnosis, graduation and treatment of the underlying pathology at an early stage. This review summarizes the potential spectrum of Post-COVID-19 pulmonary disease patterns and provides recommendations for the follow-up care of COVID-19 patients in the field of respiratory medicine.


Subject(s)
Coronavirus Infections , Lung Injury , Pandemics , Pneumonia, Viral , Pulmonary Fibrosis , Betacoronavirus , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/diagnosis , Coronavirus Infections/physiopathology , Coronavirus Infections/therapy , Humans , Lung Injury/therapy , Lung Injury/virology , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Pneumonia, Viral/physiopathology , Pneumonia, Viral/therapy , Practice Guidelines as Topic , Pulmonary Fibrosis/therapy , Pulmonary Fibrosis/virology , Pulmonary Medicine , SARS-CoV-2
19.
Eur Rev Med Pharmacol Sci ; 24(8): 4537-4538, 2020 04.
Article in English | MEDLINE | ID: covidwho-199034

ABSTRACT

At present, SARS-Cov-2 is spread all over the world, becoming a serious threat to people's health. SARS-Cov-2 has a strong infection, and the mortality rate of severe patients after infection is high, but there is no effective treatment. Mesenchymal stem cells (MSCs) have anti-inflammatory and immunomodulatory functions, which can reduce the occurrence of cytokine storm syndrome and acute respiratory distress syndrome. At the same time, MSCs can reduce the level of pulmonary fibrosis and enhance tissue injury repair. In this short report, combined with the progress of preclinical and clinical research, we comment the efficacy of MSCs in the treatment of COVID-19.


Subject(s)
Coronavirus Infections/therapy , Mesenchymal Stem Cell Transplantation , Pneumonia, Viral/therapy , Animals , Betacoronavirus , COVID-19 , Cytokines/adverse effects , Cytokines/immunology , Humans , Immunomodulation , Pandemics , Pulmonary Fibrosis/therapy , Respiratory Distress Syndrome/therapy , SARS-CoV-2
20.
Zhonghua Shao Shang Za Zhi ; 36(8): 691-697, 2020 Aug 20.
Article in Chinese | MEDLINE | ID: covidwho-8660

ABSTRACT

Coronavirus disease 2019 (COVID-19) outbroke in Wuhan, China in December 2019 and the severe acute respiratory syndrome (SARS) outbroke in Guangzhou, China in 2003 were caused by highly pathogenic coronaviruses with high homology. Since the 2019 novel coronavirus is highly contagious and spreads rapidly. It has caused negative social effects and massive economic loss globaly. Currently there is no vaccine or effective drugs. Pulmonary fibrosis is a pulmonary disease with progressive fibrosis, which is the main factor leading to pulmonary dysfunction and declined quality of life in SARS survivors after recovery. Extensive epidemiological, viral immunological and current clinical evidences support the possibility that pulmonary fibrosis may be one of the major complications in COVID-19 patients. At present there is no report on the mechanism by which COVID-19 induces pulmonary fibrosis.With the existing theoretical basis, this article focuses on discussing the possible mechanism of COVID-19 sustained lung damaging, the key role of abnormal immune mechanism in the initiation and promotion of pulmonary fibrosis, and the corresponding therapeutic measures.


Subject(s)
Betacoronavirus , Coronavirus Infections , Pandemics , Pneumonia, Viral , Pulmonary Fibrosis , COVID-19 , China , Coronavirus Infections/complications , Humans , Pneumonia, Viral/complications , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , Quality of Life , SARS-CoV-2
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