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

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BACKGROUND: Type 2 Diabetes Mellitus (T2DM) is a metabolic disease, due to the disorder of insulin function, insulin secretion, or both. Long-term hyperglycemia conditions promote endothelial dysfunction precedes to the development of multiple organ dysfunctions. Endothelial progenitor cells (EPCs) and hematopoietic stem cell (HSCs) are the key cellular effectors of postnatal neovascularization and play central role in endothelial dysfunction. However, in T2DM condition, the number of apoptotic HSCs increase, it may cause the reduction in potency and number of EPCs. In diabetes, the circulating EPCs number decrease and their functionality is impaired,  but mechanism underlie of this impairement is unknown. The purpose of this study was to examine the relationship duration diabetes with  the number and potency of EPC cells in T2DM patients controlled and poorly controlled.METHODS: Thirty-eight T2DM male patients were classified into two group based on Indonesian Society of Endocrinology/Perkumpulan Endokrinologi Indonesia (PERKENI) criteria   on T2DM.  The   first   group   was a controlled glycemic condition group (hemoglobin A1c (HbA1C) <7.0%) and the second group was a poorly controlled glycemic condition group (HbA1C >7.0%). Cluster of differentiation (CD)34+ and CD133+ expressions were used as specific marker for EPC, while quantified bright aldehyde dehydrogenase (ALDHbr) assay was used to represented the potency of EPCs.RESULTS: This study showed that in poorly controlled T2DM group the number of EPCs was lower by 24.80% (p<0.05) compared to the T2DM controlled group. Similarly, the expression of ALDHbr was lower by 43.07% (p<0.05) in poorly controlled group.CONCLUSION: There was a decrease in the number and potency of EPCs in poorly controlled T2DM patients compared to the controlled T2DM patients. There was also a strong negative correlation between the duration of diabetes and number of EPCs.KEYWORDS: ALDHbr, endothelial progenitor cells, type 2 diabetes mellitus

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

Background: There is a continuous rise in the prevalence of Diabetes Mellitus Type 2 (T2DM) worldwide and most patients are unaware of the presence of this chronic disease at the early stages. T2DM is associated with complications related to long-term damage and failure of multiple organ systems caused by vascular changes associated with glycated end products, oxidative stress, mild inflammation, and neovascularization. Among the most frequent complications of T2DM observed in about 20-40% of T2DM patients is Diabetes Nephropathy (DN). Method: Literature search was done in view of highlighting the novel application of genomics, proteomics and metabolomics, as the new prospective strategy for predicting DN in T2DM patients. Results: The complexity of DN requires a comprehensive and unbiased approach to investigate the main causes of disease and identify the most important mechanisms underlying its development. With the help of evolving throughput technology, rapidly evolving information can now be applied to clinical practice. Discussion: DN is also the leading cause of end-stage renal disease, and comorbidity independent of T2DM. In terms of the comorbidity level, DN has many phenotypes; therefore, timely diagnosis is required to prevent these complications. Currently, urine albumin-to-creatinine ratio and estimated glomerular filtration rate (eGFR) are gold standards for assessing glomerular damage and changes in renal function. However, GFR estimation based on creatinine is limited to hyperfiltration status; therefore, this makes albuminuria and eGFR indicators less reliable for early-stage diagnosis of DN. Conclusion: The combination of genomics, proteomics, and metabolomics assays as suitable biological systems that can provide new and deeper insights into the pathogenesis of diabetes, as well as to discover prospects for developing suitable and targeted interventions.

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