The role of PI3k/AKT signaling pathway in attenuating liver fibrosis: a comprehensive review

Excessive accumulation of extracellular matrix (ECM) components within the liver leads to a pathological condition known as liver fibrosis. Alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune issues, and viral hepatitis cause chronic liver injury. Exploring potential therapeutic targets and understanding the molecular mechanisms involved in liver fibrosis are essential for the development of effective interventions. The goal of this comprehensive review is to explain how the PI3K/AKT signaling pathway contributes to the reduction of liver fibrosis. The potential of this pathway as a therapeutic target is investigated through a summary of results from in vivo and in vitro studies. Studies focusing on PI3K/AKT activation have shown a significant decrease in fibrosis markers and a significant improvement in liver function. The review emphasizes how this pathway may prevent ECM synthesis and hepatic stellate cell (HSC) activation, ultimately reducing the fibrotic response. The specific mechanisms and downstream effectors of the PI3K/AKT pathway in liver fibrosis constitute a rapidly developing field of study. In conclusion, the PI3K/AKT signaling pathway plays a significant role in attenuating liver fibrosis. Its complex role in regulating HSC activation and ECM production, demonstrated both in vitro and in vivo, underscores its potential as a effective therapeutic approach for managing liver fibrosis and slowing disease progression. A comprehensive review of this field provides valuable insights into its future developments and implications for clinical applications

INFLAMMATORY BOWEL DISEASE: CLINICAL FEATURES AND MANIFESTATIONS BEYOND THE BOWEL

Inflammatory bowel disease (IBD) encompasses a spectrum of diseases, with Crohn's disease (CD) and ulcerative colitis (UC) representing the two broadest subtypes of IBD. Multiple extraintestinal manifestations (EIMs) are more frequent in (IBD); 5% –50% of the patients might be affected. The most often implicated sites of manifestations are musculoskeletal and dermatological structures. However, while some symptoms like peripheral arthritis and erythema nodosum correlate with IBD progression, others have their own course of disease like axial arthropathy, gangrenosis of the pioderma and primary sclerosic cholangitis. This review would provide a summary of the most frequent EIMs and their prevalence.                                       Peer Review History: Received 31 May 2020; Revised 7 June; Accepted 4 July, Available online 15 July 2020 Academic Editor: Dr. Muhammad Zahid Iqbal, AIMST University, Malaysia, [email protected] UJPR follows the most transparent and toughest ‘Advanced OPEN peer review’ system. The identity of the authors and, reviewers will be known to each other. This transparent process will help to eradicate any possible malicious/purposeful interference by any person (publishing staff, reviewer, editor, author, etc) during peer review. As a result of this unique system, all reviewers will get their due recognition and respect, once their names are published in the papers. We expect that, by publishing peer review reports with published papers, will be helpful to many authors for drafting their article according to the specifications. Auhors will remove any error of their article and they will improve their article(s) according to the previous reports displayed with published article(s). The main purpose of it is ‘to improve the quality of a candidate manuscript’. Our reviewers check the ‘strength and weakness of a manuscript honestly’. There will increase in the perfection, and transparency. Received file:                Reviewer's Comments: Average Peer review marks at initial stage: 5.5/10 Average Peer review marks at publication stage: 7.0/10 Reviewer(s) detail: Dr. Md. Parwez Ahmad, National Medical College, Birgunj, Nepal, [email protected] Dr. George Zhu, Tehran University of Medical Sciences, Tehran, Iran, [email protected]

Mechanistic new insights of flavonols on neurodegenerative diseases

With a large and increasing elderly population, neurodegenerative diseases such as Parkinson’s disease (PD), Huntington disease (HD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS) and Multiple sclerosis (MS) have become a major and growing health problem. During the past few decades, the elderly population has grown 2.5 % every year. Unfortunately, there are no specific therapeutic remedies available to slow the onset or development of these diseases. An aging brain causes many pathophysiological changes and is the major risk factor for most of the neurodegenerative disorders. Polyphenolic compounds such as flavonols have shown therapeutic potential and can contribute to the treatment of these diseases. In this review, evidence for the beneficial neuroprotective effect of multiple flavonols is discussed and their multifactorial cellular pathways for the progressions of age-associated brain changes are identified. Moreover, the animal models of these diseases support the neuroprotective effect and target the potential of flavonols in the treatment of neurodegenerative diseases