Peroxisome proliferator–activated receptors (PPARs) regulate energy metabolism and
hence are therapeutic targets in metabolic diseases such as type 2 diabetes and non …

Background Pancreatic β cell dysfunction and death are central in the pathogenesis of most
if not all forms of diabetes. Understanding the molecular mechanisms underlying β cell …

This cumulative body of work shows clear evidence that β-cell stress, dysfunction, and death
are harbingers of impending T1D and likely contribute to progression of disease and insulin …

Type 1 diabetes (T1D) is autoimmune destruction of the beta cells of pancreatic islets. Due
to complexity of that disease, the mechanisms leading to the tolerance breakdown are still …

Summary Type 1 diabetes (T1D) results from the progressive loss of β cells, a process
propagated by pro-inflammatory cytokine signaling that disrupts the balance between pro …

ABSTRACT Introduction Type 1 diabetes (T1D) is an autoimmune disease in which pro-
inflammatory and cytotoxic signaling drive the death of the insulin-producing β cells. This …

It is well established that distinct cell metabolic alterations strongly contribute to the
modulation of innate and adaptive immune responses. In the past decade the term …

Both type 1 and type 2 diabetes mellitus are advancing at exponential rates, placing
significant burdens on health care networks worldwide. Although traditional pharmacologic …

Islet β-cell dysfunction and aggressive macrophage activity are early features in the
pathogenesis of type 1 diabetes (T1D). 12/15-Lipoxygenase (12/15-LOX) is induced in β …

Cytokine-induced endoplasmic reticulum (ER) stress is one of the molecular mechanisms
underlying pancreatic β-cell demise in type 1 diabetes. Thrombospondin 1 (THBS1) was …