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  1. Article ; Online: Fibroblast Activating Protein: Skimming the Surface of Molecular Imaging to Assess Fibrotic Disease Activity.

    Montesi, Sydney B / Horowitz, Jeffrey C

    American journal of respiratory and critical care medicine

    2022  Volume 207, Issue 2, Page(s) 122–124

    MeSH term(s) Humans ; Lung Diseases, Interstitial/pathology ; Fibrosis ; Fibroblasts/pathology ; Molecular Imaging
    Language English
    Publishing date 2022-08-22
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202208-1638ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Corrigendum: Brief research report: impact of vaccination on antibody responses and mortality from severe COVID-19.

    Adhikari, Bindu / Bednash, Joseph S / Horowitz, Jeffrey C / Rubinstein, Mark P / Vlasova, Anastasia N

    Frontiers in immunology

    2024  Volume 15, Page(s) 1384209

    Abstract: This corrects the article DOI: 10.3389/fimmu.2024.1325243.]. ...

    Abstract [This corrects the article DOI: 10.3389/fimmu.2024.1325243.].
    Language English
    Publishing date 2024-02-28
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1384209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Serum Ferritin as a Predictor of Outcomes in Hospitalized Patients with Covid-19 Pneumonia.

    Shakaroun, Dania A / Lazar, Michael H / Horowitz, Jeffrey C / Jennings, Jeffrey H

    Journal of intensive care medicine

    2022  Volume 38, Issue 1, Page(s) 21–26

    Abstract: Purpose: ...

    Abstract Purpose:
    MeSH term(s) Humans ; COVID-19/therapy ; SARS-CoV-2 ; Respiration, Artificial ; Ventilators, Mechanical ; Ferritins ; Intensive Care Units ; Retrospective Studies
    Chemical Substances Ferritins (9007-73-2)
    Language English
    Publishing date 2022-07-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 632828-3
    ISSN 1525-1489 ; 0885-0666
    ISSN (online) 1525-1489
    ISSN 0885-0666
    DOI 10.1177/08850666221113252
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  4. Article ; Online: Releasing Tensin.

    Horowitz, Jeffrey C

    American journal of respiratory cell and molecular biology

    2017  Volume 56, Issue 4, Page(s) 417–418

    Language English
    Publishing date 2017-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2016-0417ED
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  5. Article ; Online: Investigating Matrix-Fibroblast Regulation of MicroRNAs. A Dice(r)y Proposition.

    Horowitz, Jeffrey C

    American journal of respiratory and critical care medicine

    2018  Volume 198, Issue 4, Page(s) 418–419

    MeSH term(s) DEAD-box RNA Helicases ; Fibroblasts ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis ; MicroRNAs ; Ribonuclease III
    Chemical Substances MicroRNAs ; DICER1 protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2018-04-02
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201803-0532ED
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  6. Article ; Online: How a fibroblast ages: a role for bone morphogenetic protein 4 in protecting lung fibroblasts from senescence in pulmonary fibrosis.

    Farkas, Laszlo / Horowitz, Jeffrey C / Mora, Ana L

    The European respiratory journal

    2022  Volume 60, Issue 6

    MeSH term(s) Humans ; Pulmonary Fibrosis/pathology ; Bone Morphogenetic Protein 4/metabolism ; Mitophagy ; Cellular Senescence ; Fibroblasts/metabolism ; Lung/pathology
    Chemical Substances Bone Morphogenetic Protein 4
    Language English
    Publishing date 2022-12-15
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01702-2022
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  7. Article ; Online: Brief research report: impact of vaccination on antibody responses and mortality from severe COVID-19.

    Adhikari, Bindu / Bednash, Joseph S / Horowitz, Jeffrey C / Rubinstein, Mark P / Vlasova, Anastasia N

    Frontiers in immunology

    2024  Volume 15, Page(s) 1325243

    Abstract: Introduction: While it is established that vaccination reduces risk of hospitalization, there is conflicting data on whether it improves outcome among hospitalized COVID-19 patients. This study evaluated clinical outcomes and antibody (Ab) responses to ... ...

    Abstract Introduction: While it is established that vaccination reduces risk of hospitalization, there is conflicting data on whether it improves outcome among hospitalized COVID-19 patients. This study evaluated clinical outcomes and antibody (Ab) responses to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection/vaccines in patients with acute respiratory failure (ARF) and various comorbidities.
    Methods: In this single-center study, 152 adult patients were admitted to Ohio State University hospital with ARF (05/2020 - 11/2022) including 112 COVID-19-positive and 40 COVID-19-negative patients. Of the COVID-19 positive patients, 23 were vaccinated for SARS-CoV-2 (Vax), and 89 were not (NVax). Of the NVax COVID-19 patients, 46 were admitted before and 43 after SARS-CoV-2 vaccines were approved. SARS-CoV-2 Ab levels were measured/analyzed based on various demographic and clinical parameters of COVID-19 patients. Additionally, total IgG4 Ab concentrations were compared between the Vax and NVax patients.
    Results: While mortality rates were 36% (n=25) and 27% (n=15) for non-COVID-19 NVax and Vax patients, respectively, in COVID-19 patients mortality rates were 37% (NVax, n=89) and 70% (Vax, n=23). Among COVID-19 patients, mortality rate was significantly higher among Vax vs. NVax patients (p=0.002). The Charlson's Comorbidity Index score (CCI) was also significantly higher among Vax vs. NVax COVID-19 patients. However, the mortality risk remained significantly higher (p=0.02) when we compared COVID-19 Vax vs. NVax patients with similar CCI score, suggesting that additional factors may increase risk of mortality. Higher levels of SARS-CoV-2 Abs were noted among survivors, suggestive of their protective role. We observed a trend for increased total IgG4 Ab, which promotes immune tolerance, in the Vax vs. NVax patients in week 3.
    Conclusion: Although our cohort size is small, our results suggest that vaccination status of hospital-admitted COVID-19 patients may not be instructive in determining mortality risk. This may reflect that within the general population, those individuals at highest risk for COVID-19 mortality/immune failure are likely to be vaccinated. Importantly, the value of vaccination may be in preventing hospitalization as opposed to stratifying outcome among hospitalized patients, although our data do not address this possibility. Additional research to identify factors predictive of aberrant immunogenic responses to vaccination is warranted.
    MeSH term(s) Adult ; Humans ; COVID-19 ; SARS-CoV-2 ; Antibody Formation ; COVID-19 Vaccines ; Research Report ; Vaccination ; Immunoglobulin G
    Chemical Substances COVID-19 Vaccines ; Immunoglobulin G
    Language English
    Publishing date 2024-02-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1325243
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  8. Article ; Online: Pathogenesis of pneumonia and acute lung injury.

    Long, Matthew E / Mallampalli, Rama K / Horowitz, Jeffrey C

    Clinical science (London, England : 1979)

    2022  Volume 136, Issue 10, Page(s) 747–769

    Abstract: Pneumonia and its sequelae, acute lung injury, present unique challenges for pulmonary and critical care healthcare professionals, and these challenges have recently garnered global attention due to the ongoing Sars-CoV-2 pandemic. One limitation to ... ...

    Abstract Pneumonia and its sequelae, acute lung injury, present unique challenges for pulmonary and critical care healthcare professionals, and these challenges have recently garnered global attention due to the ongoing Sars-CoV-2 pandemic. One limitation to translational investigation of acute lung injury, including its most severe manifestation (acute respiratory distress syndrome, ARDS) has been heterogeneity resulting from the clinical and physiologic diagnosis that represents a wide variety of etiologies. Recent efforts have improved our understanding and approach to heterogeneity by defining sub-phenotypes of ARDS although significant gaps in knowledge remain. Improving our mechanistic understanding of acute lung injury and its most common cause, infectious pneumonia, can advance our approach to precision targeted clinical interventions. Here, we review the pathogenesis of pneumonia and acute lung injury, including how respiratory infections and lung injury disrupt lung homoeostasis, and provide an overview of respiratory microbial pathogenesis, the lung microbiome, and interventions that have been demonstrated to improve outcomes-or not-in human clinical trials.
    MeSH term(s) Acute Lung Injury/etiology ; Acute Lung Injury/pathology ; COVID-19 ; Humans ; Pneumonia ; Respiratory Distress Syndrome/etiology ; SARS-CoV-2
    Language English
    Publishing date 2022-07-13
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20210879
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  9. Article ; Online: The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.

    Mebratu, Yohannes A / Soni, Sourabh / Rosas, Lorena / Rojas, Mauricio / Horowitz, Jeffrey C / Nho, Richard

    American journal of physiology. Cell physiology

    2023  Volume 325, Issue 3, Page(s) C565–C579

    Abstract: Idiopathic pulmonary fibrosis (IPF) is an irreversible and fatal lung disease that is primarily found in the elderly population, and several studies have demonstrated that aging is the major risk factor for IPF. IPF is characterized by the presence of ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is an irreversible and fatal lung disease that is primarily found in the elderly population, and several studies have demonstrated that aging is the major risk factor for IPF. IPF is characterized by the presence of apoptosis-resistant, senescent fibroblasts that generate an excessively stiff extracellular matrix (ECM). The ECM profoundly affects cellular functions and tissue homeostasis, and an aberrant ECM is closely associated with the development of lung fibrosis. Aging progressively alters ECM components and is associated with the accumulation of senescent cells that promote age-related tissue dysfunction through the expression of factors linked to a senescence-associated secretary phenotype (SASP). There is growing evidence that SASP factors affect various cell behaviors and influence ECM turnover in lung tissue through autocrine and/or paracrine signaling mechanisms. Since life expectancy is increasing worldwide, it is important to elucidate how aging affects ECM dynamics and turnover via SASP and thereby promotes lung fibrosis. In this review, we will focus on the molecular properties of SASP and its regulatory mechanisms. Furthermore, the pathophysiological process of ECM remodeling by SASP factors and the influence of an altered ECM from aged lungs on the development of lung fibrosis will be highlighted. Finally, recent attempts to target ECM alteration and senescent cells to modulate fibrosis will be introduced.
    MeSH term(s) Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Senescence-Associated Secretory Phenotype ; Extracellular Matrix/pathology ; Lung/pathology ; Humans ; Animals ; Extracellular Matrix Proteins/metabolism
    Chemical Substances Extracellular Matrix Proteins
    Language English
    Publishing date 2023-07-24
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00124.2023
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  10. Article ; Online: Mechanisms for the Resolution of Organ Fibrosis.

    Horowitz, Jeffrey C / Thannickal, Victor J

    Physiology (Bethesda, Md.)

    2018  Volume 34, Issue 1, Page(s) 43–55

    Abstract: Fibrosis is a dynamic process with the potential for reversibility and restoration of near-normal tissue architecture and organ function. Herein, we review mechanisms for resolution of organ fibrosis, in particular that involving the lung, with an ... ...

    Abstract Fibrosis is a dynamic process with the potential for reversibility and restoration of near-normal tissue architecture and organ function. Herein, we review mechanisms for resolution of organ fibrosis, in particular that involving the lung, with an emphasis on the critical roles of myofibroblast apoptosis and clearance of deposited matrix.
    MeSH term(s) Animals ; Apoptosis/physiology ; Extracellular Matrix/physiology ; Fibrosis/physiopathology ; Humans ; Lung/physiopathology ; Myofibroblasts/physiology
    Language English
    Publishing date 2018-12-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00033.2018
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