Ferredoxins and variants such as fladidoxins and rubredoxins are simply electron carrying protein that need to be regenerated, like the more energetic NADPH.
The key thing to remember is that redox balance is key. You cannot have electron pair accumulate so there has to be a terminal acceptor. In the case of aerobic resipration it is oxygen, in the case of iron or sulfur dissimilation it is iron(III) or sulfate, in the case of fermentation it is a small highly oxidised carbon (e.g. methanol, ethanol, butanediol, formate, acetate, propionate, lactate, succinate, fumarate). Carbon fixation requires electron pairs, which come from somewhere. The mechanism of how the carbon dioxide is assimilated can be via the Calvin cycle (plants and cyanobacteria), the Wood-Ljungdahl pathway or from the 3-hydroxypropionic cycle Prof. Fuchs described in Chloroflexi and Sulfolobus. In all three electrons come from somewhere (generally water, carbon monoxide and sulfur respectively).
The reason why there are both ferredoxins and NADPH is a tad harder to explain, but has to do with redox control and the fact that not always ferredoxin is regenerated by a NADPH reductase (also: NADH = catabolic, NADPH anabolic), but could be a fumarate reductase or similar.