Current Knowledge on the Role of Monocytes and Macrophages in the Pathogenesis of Non-AIDS Defining Events: Mechanisms, Host Factors, and Therapeutic Implications | Chapter 10 | Medical Science: Updates and Prospects Vol. 4

 

Monocytes and macrophages play a crucial role in the development of HIV infection, contributing not only to viral persistence but also to the development of non-AIDS-defining events (nADEs) in People Living with HIV (PLWH). These innate immune cells serve as long-lived viral reservoirs, driving chronic inflammation through persistent immune activation, oxidative stress, and tissue-specific damage. HIV-infected monocytes infiltrate tissues such as the cardiovascular system, liver, kidneys, and central nervous system, where they differentiate into macrophages and release pro-inflammatory cytokines (e.g., TNF-α, IL-6), reactive oxygen species (ROS), and matrix metalloproteinases (MMPs). These mediators promote endothelial dysfunction, fibrosis, and organ damage, underpinning conditions like atherosclerosis, neurocognitive disorders, and hepatorenal disease. Emerging evidence highlights the importance of macrophage polarisation (M1/M2 imbalance) and epigenetic modifications in sustaining inflammation, even during antiretroviral therapy (ART). Besides persistent immune activation, the ability of these cells to cause tissue-specific damage is significantly influenced by host genetic factors, such as polymorphisms in the APOL1 and CCL2 genes, which can determine the severity of end-organ diseases like HIV-associated nephropathy. Additionally, epigenetic reprogramming of monocytes and macrophages—triggered by HIV proteins and the inflammatory environment—establishes a lasting pro-inflammatory state that remains despite ART. This reprogramming, marked by changes in histone modifications and DNA methylation, sustains mechanisms of tissue damage. Understanding these processes and their interaction with host factors provides critical insights for developing targeted treatments, including immunomodulators, antioxidants, and strategies for reservoir elimination. This review summarises current knowledge on how monocytes and macrophages contribute to the pathogenesis of nADEs. It explores potential new therapeutic approaches to reduce chronic inflammation and enhance clinical outcomes in PLWH.

 

 

Author(s) Details

Samuel Adinoyi Adavba
Kaduna State University, Kaduna, Nigeria.

 

Please see the book here :- https://doi.org/10.9734/bpi/msup/v4/6480

 

Addressing Racial Disparities in Quadruple-Negative Breast Cancer: Insights Into Aggressive Biology, Therapeutic Targets, and Prevention Strategies |Chapter 3 | Disease and Health: Research Developments Vol. 7

Black/African-American (AA) women, relative to their White/European-American (EA) counterparts, experience disproportionately high breast cancer mortality. Central to this survival disparity, Black/AA women have an unequal burden of aggressive breast cancer subtypes, such as triple-negative breast cancer (ER/PR-, HER2-wild type; TNBC). TNBC is inherently more clinically aggressive than the other breast cancer subtypes as evidenced by the higher frequency of metastasis and recurrence within 5 years of diagnosis. While TNBC has been well characterized, recent studies have identified a highly aggressive androgen receptor (AR)-negative subtype of TNBC, quadruple-negative breast cancer (ER/PR-, HER2-wildtype, AR-; QNBC). QNBCs are significantly more aggressive than AR-positive TNBCs. QNBC is increasingly recognized as an aggressive, hard-to-treat breast cancer subtype. Similar to TNBC, QNBC disproportionately impacts Black/AA women and likely plays an important role in the breast cancer survival disparities experienced by Black/AA women. Here, a discussion has been developed on the racial disparities of QNBC and molecular signaling pathways that may contribute to the aggressive biology of QNBC in Black/AA women. This study intends to spotlight potential prevention and therapeutic targets for Black/AA QNBC; ultimately the goal of this study is to provide greater insight into reducing the breast cancer survival burden experienced by Black/AA women. Non-genetic risk factors include lifestyle, socioeconomic status, access to quality oncological care, reproductive factors, anthropometrics, and comorbidities have long been reported to contribute to the gap in survival rates between Black/AA and White/EA women with breast cancer. The Potential Role of Non-Genetic Risk Factors in the Racially Disparate Burden in QNBC is also discussed here. Addressing the racial disparity in the highly aggressive breast cancer subtype, QNBC could significantly contribute to reducing the racially disparate burden of breast cancer.

 

Author (s) Details

 

Nikita Jinna
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Tijana Jovanovic- Talisman
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Mark LaBarge
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Rama Natarajan
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Rick Kittles
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

 

Christopher Sistrunk
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Padmashree Rida
Novazoi Theranostics, Salt Lake City, UT 84105, USA.

 

Victoria L. Seewaldt
City of Hope Comprehensive Cancer Center, Duarte, CA 91010, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v7/4732

Type 2 Diabetes and Epigenetics: A Comprehensive Review | Chapter 5 | Advancement and New Understanding in Medical Science Vol. 9

Type 2 Diabetes is one of the major public health issues and a complex metabolic disorder strongly associated with genetic predisposition influenced by environmental factors and epigenetic regulation. Around 537 million people were diagnosed as diabetic in 2021 worldwide and it is predicted that the number will rise to 578 million by 2030, and 700 million by 2045. This review paper illustrated the role of epigenetics in the pathogenesis, progression, and detection of Type 2 Diabetes. A review study was performed for the articles published in English from 2000-2023 using Pub Med, and Google Scholar databases. Main underlining mechanisms of Type 2 Diabetes were identified: insulin resistance in the peripheral tissue and disintegrated insulin secretion. Epigenetics is “the study of changes in the gene functions that are mitotically and/or meiotically heritable and that do not entail a change in DNA sequence. Genome Wide Association Studies suggested that epigenetic regulation such as DNA methylation, Histone modification, microRNA strongly co-relates the development and progression of Type 2 Diabetes. Altered DNA methylation patterns in pancreatic islets, skeletal muscle, adipose tissue, from diabetic subjects compare to normal subjects was also found. Other risk factors like obesity, age, gender, impaired glucose tolerance, periconception and intrauterine environment may also have been linked with the possibilities of epigenetic changes. Lifestyle, socioeconomic condition, food habits are contributing to obesity and Type 2 Diabetes. Every year 2.8 million people die worldwide due to obesity and its complications. Epigenetics plays a crucial role by modifying the gene expression and establishing a relationship between the environment and genetic factors. Understanding the epigenetic mechanisms contributing to the development of Type 2 Diabetes is still limited.

Author(s) Details:

Abhijeet Roy,
Institute for Biomedical Sciences, Georgia State University, GA, USA and Center for Non-Communicable Diseases and Nutrition, BRAC James P Grant School of Public Health, BRAC University, Bangladesh.

Please see the link here: https://stm.bookpi.org/ANUMS-V9/article/view/13624

miRNA and Cancer| Chapter 16 | New Frontiers in Medicine and Medical Research Vol. 15

MicroRNAs are small non-coding RNA molecules that play a key function in gene control. Translational repression and even cancer can result from issues with miRNA biogenesis. MicroRNAs can function as tumour suppressors or oncogenes. The function of microRNAs is influenced by a variety of circumstances. A network of oncogenes, microRNAs, and tumour suppressor genes (TSG) has an impact on not only normal cellular processes but also tumorigenesis. Thus, a better understanding of the regulatory variables and network can aid in the re-discovery of therapeutic targets in cancer.

Author (S) Details

Susinjan Bhattacharya

Department of Biotechnology, Jaypee Institute of Information Technology, A-10, Sector 62, Noida, Uttar Pradesh, India.

View Book :- https://stm.bookpi.org/NFMMR-V15/article/view/3876