Stem Cell Studies in Cardiovascular Biology and Medicine: A Possible Key Role of Macrophages

Kawaguchi, Nanako; Nakanishi, Toshio

doi:10.3390/biology11010122

Cited by 7 publications

(4 citation statements)

References 124 publications

(141 reference statements)

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“…The ACE2/Ang 1-7)/MasR axis plays an important role in the biology of vasculogenic progenitor cells, hematopoietic stem cells, cardiomyocytes and dental stem cells [10,24,25]. Ang (1-7) improves pancreatic β-cell function and long-term Ang (1-7) administration in vivo affects insulin secretion from islets [26].…”

Section: Discussionmentioning

confidence: 99%

Angiotensin 1–7 Stimulates Proliferation of Lung Bronchoalveolar Progenitors—Implications for SARS-CoV-2 Infection

Ciechanowicz

Lay

Paulino

et al. 2022

Cells

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SARS-CoV2 infection leads to severe lung damage due to pneumonia and, in more severe cases, leads to acute respiratory distress syndrome, or ARDS. This affects the viability of bronchoalveolar cells. An important role in the pathogenesis of these complications is the hyperactivation of the renin-angiotensin-aldosterone (RAA) pathway and induction of cytokine storm that occurs in an Nlrp3 inflammasome-dependent manner. To shed more light on the susceptibility of lung tissue to SARS-CoV2 infection, we evaluated murine bronchioalveolar stem cells (BASC), alveolar type II cells (AT2), and 3D-derived organoids expression of mRNA encoding genes involved in virus entry into cells, components of RAA, and genes that comprise elements of the Nlrp3 inflammasome pathway. We noticed that all these genes are expressed by lung alveolar stem cells and organoids-derived from these cells. Interestingly, all these cells express a high level of ACE2 that, on the one hand, serves as an entry receptor for SARS-CoV2 and, on the other, converts angiotensin II into its physiological antagonist, angiotensin 1–7 (Ang 1–7), which has been reported to have a protective role in lung damage. To shed more light on the role of Ang 1–7 on lung tissue, we exposed lung-derived BASC and AT2 cells to this mediator of RAA and noticed that it increases the proliferation of these cells. Based on this, Ang 1–7 could be employed to alleviate the damage to lung alveolar stem/progenitor cells during SARS-CoV2 infection.

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Section: Discussionmentioning

confidence: 99%

Angiotensin 1–7 Stimulates Proliferation of Lung Bronchoalveolar Progenitors—Implications for SARS-CoV-2 Infection

Ciechanowicz

Lay

Paulino

et al. 2022

Cells

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“…This mechanism has been deemed responsible for the restorative processes associated with cell therapy, including positive myocardial remodelling, cardioprotection, neovascularization, and neo-myogenesis 85 ( Figure 2 ). The now emerging paradigm is that exogenous cells may exert most of their beneficial actions via an immune-modulation, in particular recent studies have highlighted the emerging role of macrophages in triggering cell regeneration 28 , 86 The above considerations bring into question the contraposition of autologous vs allogenic stem cell therapy. Most of the studies seem to agree that if the paracrine effect is what a cell therapy approach has to achieve, then allogenic cells are the strategy to prefer.…”

Section: Gaps In Evidencementioning

confidence: 99%

Myocardial regeneration protocols towards the routine clinical scenario: An unseemly path from bench to bedside

Salerno

Marino

et al. 2022

eClinicalMedicine

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“…For example, many in vitro disease models have been established [ 15 , 16 , 17 ] since induced pluripotent stem cells (iPSCs) were first developed by Takahashi and Yamanaka [ 18 , 19 ]. However, the immaturity of cardiomyocytes derived from iPSCs has been reported [ 20 , 21 ]. This is one of the problems associated with iPSC-derived cardiomyocytes, with symptoms often appearing after birth.…”

Section: Introductionmentioning

confidence: 99%

Animal Disease Models and Patient-iPS-Cell-Derived In Vitro Disease Models for Cardiovascular Biology—How Close to Disease?

Kawaguchi

Nakanishi

2023

Biology

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Currently, zebrafish, rodents, canines, and pigs are the primary disease models used in cardiovascular research. In general, larger animals have more physiological similarities to humans, making better disease models. However, they can have restricted or limited use because they are difficult to handle and maintain. Moreover, animal welfare laws regulate the use of experimental animals. Different species have different mechanisms of disease onset. Organs in each animal species have different characteristics depending on their evolutionary history and living environment. For example, mice have higher heart rates than humans. Nonetheless, preclinical studies have used animals to evaluate the safety and efficacy of human drugs because no other complementary method exists. Hence, we need to evaluate the similarities and differences in disease mechanisms between humans and experimental animals. The translation of animal data to humans contributes to eliminating the gap between these two. In vitro disease models have been used as another alternative for human disease models since the discovery of induced pluripotent stem cells (iPSCs). Human cardiomyocytes have been generated from patient-derived iPSCs, which are genetically identical to the derived patients. Researchers have attempted to develop in vivo mimicking 3D culture systems. In this review, we explore the possible uses of animal disease models, iPSC-derived in vitro disease models, humanized animals, and the recent challenges of machine learning. The combination of these methods will make disease models more similar to human disease.

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Stem Cell Studies in Cardiovascular Biology and Medicine: A Possible Key Role of Macrophages

Cited by 7 publications

References 124 publications

Angiotensin 1–7 Stimulates Proliferation of Lung Bronchoalveolar Progenitors—Implications for SARS-CoV-2 Infection

Angiotensin 1–7 Stimulates Proliferation of Lung Bronchoalveolar Progenitors—Implications for SARS-CoV-2 Infection

Myocardial regeneration protocols towards the routine clinical scenario: An unseemly path from bench to bedside

Animal Disease Models and Patient-iPS-Cell-Derived In Vitro Disease Models for Cardiovascular Biology—How Close to Disease?

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