Introduction: Each cell in human body is assigned with a specialized function to perform.  Before a cell becomes specialized, it is a stem cell. Stem cell research and therapy is progressing dramatically these days. Stem cell therapy holds enormous treatment potential for many diseases which currently have no or limited therapeutic options. Unfortunately, this potential also comes with side-effects. In this review, the positive and negative effects of regulation of stem cells will be explained.Content: Stem cells are undifferentiated cells that have potential to develop into many different cell types in the body during early life and growth. The type of stem cells are embryonic stem cells, induced pluripotent stem cells, somatic stem cells, foetal stem cells and mesenchymal stem cells. Stem cell transplantation is one form of stem cell therapy, it comes with different sources, and those are autologous and allogenic transplantation stem cells. In an autologous transplant, a patient’s own blood-forming stem cells are collected, meanwhile in an allogeneic transplant, a person’s stem cells are replaced with new stem cells obtained from a donor or from donated umbilical cord blood.Summary: Its abilities to maintain undifferentiated phenotype, self-renewing and differentiate itself into specialized cells, give rise to stem cell as a new innovation for the treatment of various diseases. In the clinical setting, stem cells are being explored in various conditions, such as in tissue repair and regeneration and autoimmune diseases therapy. But along with its benefit, stem cell therapy also holds some harm. It is known that the treatment using stem cell for curing and rehabilitation has the risk in tumor formation.

Autophagy is essential in cell death decisions and can protect cells by preventing them from undergoing apoptosis. Autophagy contributes to a variety of physiological processes, including cell differentiation and various functions in embryogenesis. Some studies reported that the expressions of autophagy-related (Atg) proteins are found in placentas. This review article was focusing on the autophagy process and some Atg proteins which are involved in human placentation, especially in preeclampsia cases, since it has been well known that abnormal placentation and placenta dysfunction has crucial role in its development. Preeclampsia cannot be related to a single cause and the underlying mechanism of it is still not clearly understood. Recent hypothesis regarding the cause of preeclampsia is more focused on the inadequate trophoblast invasion and placentation. Scientists also suggested that other mechanism might be associated with this condition in preeclampsia, which is autophagy. Autophagy is a mechanism that essential for cellular remodeling which occurs during the development of multicellular organisms in the special process, by expressing an “eat-me” signal and cleared by neighboring cells. In preeclampsia patients, autophagy has an important role in trophoblast function under physiologically low oxygen conditions. The activation of autophagy in preeclampsia is shown by the different level of abundance of key protein of the Atg pathway. Some Atg proteins known to be related to preeclampsia are Beclin-1, LC3, and p62.Keywords: Atg proteins, cell death, embryogenesis, placentation Peran Autofagi dalam PreeklampsiaAbstrakAutofagi memiliki peran yang penting dalam keputusan kematian sel dan dapat melindungi sel dengan cara mencegahnya mengalami apoptosis. Autofagi berkontribusi pada berbagai proses fisiologis, termasuk diferensiasi sel dan berbagai fungsi dalam embriogenesis. Beberapa penelitian melaporkan bahwa ekspresi protein Atg ditemukan di plasenta. Artikel review ini berfokus pada proses autofagi dan beberapa protein autophagy-related (Atg) yang terlibat dalam plasentasi, terutama pada kasus preeklampsia, karena telah diketahui bahwa plasentasi abnormal dan disfungsi plasenta memiliki peran yang penting dalam perkembangan. Preeklampsia tidak dapat dikaitkan dengan satu penyebab saja, dan mekanisme yang mendasarinya masih belum dipahami secara jelas. Hipotesis terbaru mengenai penyebab terjadinya preeklampsia lebih terfokus pada invasi trofoblast yang tidak memadai dan kesalahan plasentasi. Para ilmuwan juga menyarankan bahwa mekanisme lain yang mungkin terkait dengan kondisi ini adalah autofagi. Autofagi adalah mekanisme yang penting untuk pemodelan ulang seluler yang terjadi selama perkembangan organisme multiseluler dalam proses khusus, dengan mengekspresikan sinyal “makan-saya” dan kemudian dibersihkan oleh sel tetangga. Pada pasien preeklampsia, autofagi memiliki peran penting dalam fungsi trofoblas di bawah kondisi oksigen rendah. Pengaktifan autofagi pada preeklampsia ditunjukkan oleh perbedaan tingkat kelimpahan protein utama dari pathway Atg. Beberapa protein Atg yang diketahui terkait dengan preeklampsia adalah Beclin-1, LC3, dan p62.Kata kunci: Embriogenesis, kematian sel, plasentasi, protein Atg

Stroke is a leading cause of death and long-term disability. This due to the ischemic event that cause by embolism of blockage blood flow. Thrombolytic agent plasminogen activator (tPA) is the only treatment approved by FDA. However, the used of tPA is limited to the short time window period. Neural stem cells (NSCs) show the potential to repair neuronal damage naturally after stroke. However, isolating NSCs is a challenging process due to the limitations of the method and its invasiveness. Some studies that had used mesenchymal stem cell (MSCs) as the main source of stem cell for therapy show that MSCs have the potency to differentiate into NSCs. in vitro, a differentiation process from MSC to NSC has been developed by combining the supplement or growth factor needed in the culture media.Keywords: stem cells, neuron stem cell, mesenchymal stem cell, stroke, trans-differentiation

BACKGROUND: The mechanism of aging goes along with age, one of which is characterized by cellular senescent, which occurs mostly in adipose tissue. Adipose tissue is the site of accumulation of large cell senescent, in the regulation of obesity and aging. Proteins p53 is marker for cell senescent, which are also known to induce inflammation. This study was aimed to determine the relationship between circulating protein p53 and high sensitivity C-reactive protein (hsCRP) in central obese men with inflammaging.METHODS: The study design is an observational study with cross-sectional approach. The subjects were 75 central obese men (waist circumference/WC > 90 cm), aged ≥ 45 years old. Subjects were divided into 2 age groups, those are middle age group: 45-59 years old (50.7%) and elderly group: ≥ 60 years old (49.3%). Examination of circulating p53 was done using enzyme-linked immunosorbent assay (ELISA) method, and the hsCRP examination was done by chemiluminescent method.RESULTS: It was found that there was a correlation between circulating p53 and hsCRP in elderly (r=-0.414; p<0.05) but not in middle age (r=-0.127; p=0.449).CONCLUSION: From this study, it is assumed that more senescence cells in elderly are resulting in increased chronic inflammation.KEYWORDS: aging, senescent, inflammaging, protein p53, hsCRP

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR)-γ, or also known as nuclear receptor subfamily 1 group C member 3 (NR1C3), is a PPAR which serves as master regulator of adipocytes differentiation, and plays an important role in lipid metabolism or adipogenesis. Recent study showed that PPAR-γ is expressed in most tissue and also has critical impact in many metabolic homeostasis disorders.CONTENT: Dysregulation of PPAR-γ is correlated to the development of obesity, type 2 diabetes, atherosclerosis, cardiovascular disease, acute kidney injury, autoimmune disease, gastrointestinal disease and Alzheimer’s disease. Abundant number of new emerging compounds, with in vitro and in vivo effectiveness as natural and synthetic agonists of PPARs, are investigated, developed and used as the treatment of metabolic disorders of glucose and/or lipid and other diseases.SUMMARY: Based on all studies explanation, targeting PPAR-γ is proven to be a good therapeutic method for reducing negative effect of several metabolic homeostasis disorder. Now, many natural and synthetic agonists of PPARs are used as the treatment of metabolic disorders of glucose and/or lipid or another metabolic homeostasis disorder. Such agonists have different properties and specificities for individual PPARs receptors, different absorption and distribution, and distinctive gene expression profiles, which ultimately lead to different clinical outcomes.KEYWORDS: PPAR-γ, dysregulation, agonist, adipogenesis, metabolic disorder, homeostasis